Cardiovascular Endocrinology Group

Research Overview

Heart failure occurs when the heart is unable to pump sufficient blood due to ‘stiffening’ of the myocardium caused by increased tissue fibrosis and changes in myocardial passive stiffness. Tissue injury, with chronic inflammation and fibrogenesis, results in disruption of normal tissue architecture and function and can progress to organ failure. Therapeutic options for chronic fibrosis, in the heart and other organs, are severely limited.

A new biology for the mineralocorticoid receptor (MR)

It was believed that chronic MR activation resulted in high blood pressure only, and increased Angiotensin II signalling caused fibrosis. However, we have shown that mineralocorticoids cause cardiac fibrosis via direct actions in the heart, contributing to large-scale clinical trials that established a major role for MR signalling in heart failure.

The 'textbook' model of MR biology is flawed

The MR controls numerous processes in non-renal tissues. Understanding MR mechanisms of action in these tissues is a prerequisite for future discovery of drugs that are selective for MR in the heart. Accordingly, we have developed a suite of tissue-specific MR null mice and genetically modified cell lines in order to understand this new MR biology as it relates to heart disease. Outcomes of this laboratories work identifying cell selective pathways, conformational changes and ligand dependent protein interactions for the MR have led to engagement with industry and together with clinical testing of preclinical data have created a pipeline for translating new therapies for cardiac fibrosis and heart failure.

Ongoing projects seek to identify novel mechanisms of MR signalling in macrophages and cardiomyocytes to generate new directions for the development of a selective MRA for cardiac fibrosis.

Projects include:

  • Identify MR dependent mechanisms in tissue macrophages that regulate inflammatory and fibrotic pathways and determine the function of novel MRA signalling in vivo in clinical studies.
  • Define MR and molecular clock interactions to provide new knowledge for MR actions in cardiomyocytes (i.e. disruption of the molecular clock as a driver for cardiac fibrosis).
  • Engineer and test novel MR modulating compounds for cardiac fibrosis and inflammation that may also have fewer side effects.

Circadian disruption and CVD

Circadian disruption is increasingly recognised as a contributor to cardiometabolic diseases, including obesity, type 2 diabetes, hypertension, and cardiovascular disease (CVD). Epidemiological studies have consistently linked shift work, irregular sleep patterns, and social jet lag to increased cardiometabolic risk. Shift workers, exhibit higher incidences of insulin resistance, dyslipidaemia, and myocardial infarction compared to daytime workers. Experimental models support these findings, showing that disruption of circadian genes (e.g., Clock, Bmal1, Per) in the peripheral tissues of mice leads to impaired glucose tolerance, increased adiposity, and elevated blood pressure. Adrenal corticosteroids (cortisol) and their tissue receptors (GR) are established entrainment signals for peripheral tissue clocks and their disruption can promote circadian dysregulation at the tissue level. The host lab has recently identified a second hormone receptor, the MR as contributing to circadian entrainment in peripheral tissues.

Mechanistically, circadian rhythms regulate key metabolic processes through central and peripheral clocks. The central pacemaker in the suprachiasmatic nucleus synchronizes peripheral clocks in tissues such as the liver, adipose tissue, and heart. Disruption of these rhythms can desynchronize metabolic processes, impair hormonal signalling (e.g., insulin, leptin, cortisol), and alter lipid and glucose homeostasis. Circadian misalignment also contributes to chronic inflammation and endothelial dysfunction, both central to atherogenesis and metabolic syndrome. Moreover, recent data implicate the gut microbiome and its diurnal oscillations in mediating metabolic effects of circadian disruption.

Despite growing insights, several key questions remain:

To what extent are these effects modulated by sex, age, and genetic background?

How do specific circadian disruptions (e.g., light exposure vs. meal timing vs. sleep loss) differentially affect metabolic outcomes.

How does circadian disruption at the tissue level contribute to the progression of chronic disease?

The goal of the studies outlined are to understand how circadian disruption promotes CVD and to determine new strategies for circadian based, e.g., timed feeding, light therapy, melatonin or chronotherapy, to meaningfully reduce the risk of CVD.

In sum, while strong clinical and preclinical evidence links circadian disruption to cardiometabolic disease, causal mechanisms and therapeutic strategies are still being elucidated. Understanding how circadian rhythms interface with metabolic pathways may offer novel preventive and treatment approaches in a world increasingly out of sync.

Investigating the Role of Circadian Disruption in Cardiometabolic Disease

Disruption of the body’s natural circadian rhythms is increasingly recognized as a risk factor for a wide range of cardiometabolic diseases, including obesity, type 2 diabetes, high blood pressure, and cardiovascular disease (CVD). Large-scale studies have shown that individuals with irregular sleep patterns such as shift workers are more likely to experience insulin resistance, abnormal cholesterol levels, and heart attacks than those with regular daytime schedules.

Animal studies help explain these findings. Mice with genetic disruptions in key circadian clock genes (such as Clock, Bmal1, and Per) develop problems with glucose metabolism, gain excess fat, and have elevated blood pressure. Hormones like cortisol, which follow a daily rhythm and act through receptors such as the glucocorticoid receptor (GR), help synchronize internal clocks in tissues like the liver, fat, and heart. The host lab has recently identified a second hormone receptor, the mineralocorticoid receptor (MR), as another important player in this circadian timing system.

Circadian rhythms influence nearly all aspects of metabolism. The brain’s master clock, located in the suprachiasmatic nucleus (SCN), coordinates with peripheral clocks in organs to maintain proper timing of processes like glucose regulation and lipid metabolism. When these rhythms are disrupted through altered sleep, light exposure, or meal timing it can lead to hormonal imbalances, chronic inflammation, and blood vessel dysfunction, all of which contribute to metabolic syndrome and atherosclerosis.

This project is part of a larger study and will evaluate how circadian misalignment contributes to cardiometabolic disease progression, with a focus on the underlying mechanisms and potential interventions in peripheral tissues. Key research questions include:

  • How do sex, age, and genetic factors influence the impact of circadian disruption?
  • What are the specific effects of different types of disruption (e.g., light at night vs. irregular meals vs. sleep loss)?
  • How does tissue-level disruption of circadian rhythms promote chronic disease?

Techniques will include RNA and protein isolation, RT PCR, western blot, immunostaining if relevant, R program for analysis of adipose and potentially other tissues and will involve the use of tissue from short term physiological challenge models and a model of cardiometabolic disease. Outcomes will help to identify key pathways that are dysregulated by circadian disruption in peripheral tissues that may contribute to cardiovascular disease. While evidence linking circadian disruption to metabolic disease is strong, more research is needed to define causal pathways and develop effective treatments. This project aims to contribute to that growing field and uncover new ways to promote health in an increasingly 24/7 society.

Sleep, Circadian Rhythms, and Aldosterone Regulation in Cardiovascular Risk

Aldosterone, a key regulator of blood pressure and electrolyte balance, is secreted in a circadian pattern that peaks in the early morning, aligned with cortisol release. This rhythmic regulation is mediated by the mineralocorticoid receptor (MR), whose expression and activity are under circadian control. Recent preclinical studies from our group reveal a bidirectional relationship between the circadian clock and MR signalling: not only do clock genes influence MR expression, but MR activation feeds back to regulate circadian gene rhythms.

Early translational research suggests that behavioural cues, such as meal timing, can shift aldosterone secretion and alter the aldosterone-to-renin ratio (ARR). However, little is known about how sleep timing and quality, which are a critical circadian input, impact regulation of aldosterone production in humans. Given the known associations between poor sleep, disrupted cortisol rhythms, and cardiometabolic risk, this project will investigate whether sleep behaviours also modulate aldosterone patterns and contribute to cardiovascular risk.

The primary goal of this project is to determine how objectively measured sleep timing and quality influence morning serum aldosterone, renin, and the ARR in a community-based adult cohort. This project will also assess associations between sleep parameters and morning cortisol and cortisone levels and examine whether sleep-related hormonal variations are linked to early cardiovascular markers such as elevated blood pressure or increased left ventricular mass. If time permits, we will explore if the cortisol:cortisone ratio (a marker of 11β-HSD enzyme activity) varies with sleep timing and quality, and whether this correlates with cardiovascular risk indices.

Data analysis will use: Sleep measurements from wrist-worn actigraphy over a 7-day period to collect objective data on sleep onset, offset, duration, and fragmentation; Serum hormone levels: fasting morning serum samples to measure aldosterone, renin, cortisol, and cortisone; and calculated indices: e.g. the aldosterone-to-renin ratio (ARR) and cortisol-to-corticosteone ratio to indicate 11β-HSD2 activity. We will work with the bioinformatics team to perform statistical modelling including multivariable regression models to test associations between sleep metrics and hormone levels, adjusting for confounders such as age, sex, BMI, sodium intake, and blood pressure.

Interaction Testing: Evaluate interaction terms to determine whether poor sleep exacerbates the hypertensive effects of elevated aldosterone.

Bioinformatic skills are required: Students will be expected to engage with population-level datasets and perform hormone-sleep correlation analyses. Prior experience or willingness to develop skills in statistical programming (e.g., R or Python), data visualisation, and the use of bioinformatic tools for hormonal and cardiovascular phenotype analysis is essential.

This project will be among the first to translate mechanistic insights from animal models of MR–circadian crosstalk into human populations. By identifying sleep characteristics that modulate aldosterone and MR activity, the project may help define new behavioural targets—such as improving sleep timing or duration—to reduce cardiovascular risk, especially in individuals prone to mineralocorticoid excess (e.g., primary aldosteronism).

Outcomes will inform chronobiological strategies for hypertension and cardiovascular risk management and guide future studies examining MR and circadian gene expression in peripheral tissues. The project provides a unique opportunity to bridge basic circadian biology, hormonal regulation, and cardiovascular epidemiology through an integrated translational research approach.

Staff

  • Assoc Prof Morag Young Group Leader
  • Ms Monica Kanki PhD Student
  • Mr Nikshay Karthigans PhD Student
  • Mr Seamus Heanue BMedSci Student
  • Mr John Soo Master's Student
  • Ms Rizqa Putri BMedSci Student
  • Mr Ryan Kissick Honours Student
  • Mr Viet Ho Quoc PhD Student

Cosupervised PHD students (Monash, Endocrine Fellows)

  • Dr Renata Libianto
  • Dr Sonali Shah

Collaborators

  • Prof Mike Inouye (Baker Heart and Diabetes Institute, Cambridge University UK)
  • Prof David Ray (Oxford University UK)
  • Prof Julie McMullen (Baker Heart and Diabetes Institute)
  • A/Prof David Greening (Baker Heart and Diabetes Institute
  • A/Prof Jun Yang (Monash University, Hudson Institute)
  • A/Prof Kegan Monaghetti (Baker Heart and Diabetes Institute, University of Melbourne)
  • Prof Tim Cole (Baker Heart and Diabetes Institute, Cambridge University)
  • Prof Mike Inouye (Monash University)
  • Prof Peter Fuller (Hudson Institute)

Funding

  • 2020-2025 A/Prof Morag Young, Alice Baker and Eleanor Shaw Gender Equity Fellowship. $980,000 Baker Trust.
  • 2020 A/Prof Morag Young, Impact Philanthropy Application Program - IPAP2020/0235. Engineering safer therapies for heart failure; protection for hard-to-treat groups. $89,000.
  • 2020 A/Prof Morag Young and AProf Natalie Hannan, Baker University of Melbourne Seed Fund. Risk of heart failure in women following preeclampsia: is prevention possible? $200,000
  • 2021 A/Prof Morag Young, AProf Cristian Carvajal, Dr Damian Romero and Dr Jun Yang. FONDECYT Role of mineralocorticoid receptor and exosomes in endocrine hypertension and cardio-renal communication. $20,000.
  • 2022 A/Prof Morag Young Commercial Development Seed Funding Baker Heart and Diabetes Institute $50,000
  • 2022 A/Prof Morag Young NHF Vanguard Grant, $75,000 Engineering safer therapies for heart failure - protection for hard-to-treat groups
  • 2022 A/Prof Morag Young Discovery Domain Seed Fund Baker Heart and Diabetes Institute for development of preclinical model of HFpEF $50,000
  • 2022 A/Prof Morag Young and Dr Kegan Monaghetti Collaborative Seed Fund University of Melbourne. Development of a wholistic blood test for cardiometabolic health $100,000
  • 2023-2025 A/Prof Morag Young ARC - A new biology for the mineralocorticoid receptor - circadian time and the heart $430,000

Research Outcomes

  1. Chi-Sheng Hung, Yi-Yao Chang, Cheng-Hsuan Tsai, Che-Wei Liao, Shih-Yuan Peng, Bo-Ching Lee, Chien-Ting Pan, Xue-Ming Wu, Zheng-Wei Chen, Vin-Cent Wu, Cho-Hua Wan, Morag J Young, Chia-Hung Chou, Yen-Hung Lin, TAIPAI Study Group (2022). Aldosterone suppresses cardiac mitochondria. Translational Research. 239:58-70. IF = 8.499.
  2. Jordan H Lai, Stella May Gwini, Gang Chen, Katrina M Long, Grant Russell, Markus P Schlaich, Michael Stowasser, Morag J Young, Peter J Fuller, Trevor A Mori, Martin Wolley, Christopher M. Reid, Jun Yang (2022). Willingness to be tested for a secondary form of hypertension: a survey of the Australian general community. Internal Medicine Journal IMJ-0591-2022.R1 Accepted Oct 2022
  3. Pravik Solanki, Stella May Gwini, Renata Libianto, Genevieve Gabb, Jimmy Shen, Morag J Young, Peter J Fuller, Jun Yang (2022). Risky Business: Calculated Cardiovascular Risk Underestimates Real Risk in Hypertensive Patients with Primary Aldosteronism. BMJ Open. Accepted 26th Oct 2022

Research Publications

  1. Young, M.J., Fullerton, M., Dilley, R. and Funder, J.W. (1994). Mineralocorticoids, hypertension and cardiac fibrosis. Journal of Clinical Investigation 93: 2578-2583. IF= 16.915 Citations: 549
  2. Young, M.J., Head, G. and Funder, J.W. (1995). Determinants of cardiac fibrosis in experimental hypermineralocorticoid states. American Journal of Physiology 269: E657-E662. IF=3.881 Citations: 311
  3. Young, M.J. and Funder, J.W. (1996). The renin-angiotensin-aldosterone system in experimental mineralocorticoid-salt induced fibrosis. American Journal of Physiology 271: E883-E888.
  4. Dellovade, T.L., Young, M.J., Ross, E.P., Henderson, R., Caron, K.M., Parker, K.L. and Tobet, S.A. (2000). Disruption of the gene encoding SF-1 alters the distribution of hypothalamic neuronal phenotypes. Journal of Comparative Neurology 423: 579-589.
  5. Young, M.J., Clyne, C.D., Cole, T.C. and Funder, J.W. (2001). Cardiac steroidogenesis in the normal and failing heart. Journal of Clinical Endocrinology and Metabolism 86: 5121-5126.
  6. Majdic, G., Young, M.J., Gomez-Sanchez, E., Anderson, P., Szczepaniak, L., Dobbins, R., McGarry, J.D. and Parker, K.L. (2002). SF-1 knockout mice are a novel genetic model of hypothalamic obesity. Endocrinology 143: 607-614. IF=4.993 Citations: 310 2.68
  7. Young, M.J., Moussa, L., Dilley, R. and Funder, J.W.  (2003). Early inflammatory responses in experimental cardiac hypertrophy and fibrosis: effects of 11bhydroxysteroid dehydrogenase inactivation. Endocrinology 144: 1121-1125. IF=4.993 Citations: 144 4.98
  8. Sofi, M., Young, M.J., Papamakarios, T., Simpson, E.R. and Clyne, C.D. (2003). Role of CRE-binding protein (CREB) in aromatase expression in breast adipose. Breast Cancer Research and Treatment 79: 399-407. IF= 4.453 Citations: 81
  9. Young, M.J. and Funder, J.W. (2003). Mineralocorticoid action and sodium-hydrogen exchange: studies in experimental cardiac fibrosis. Endocrinology 144:3848-51 IF=4.993 Citations:61
  10. Young, M.J. and Funder, J.W. (2004). Eplerenone, but not steroid withdrawal, reverses cardiac fibrosis in deoxycorticosterone/salt-treated rats. Endocrinology; 145:3153-7 IF=4.993 Citations:131
  11. Lam, E.Y.M., Fuller, P.J., Nikolic-Paterson, D.J., Funder, J.W. and M.J. Young (2006). Mineralocorticoid receptor blockade but not steroid withdrawal reverses renal fibrosis in DOC/salt rats. Endocrinology.147:3623-9.IF=4.993 Citations: 46
  12. Rickard, AJ., Funder, JW., Fuller, PJ., and M.J. Young (2006). The role of the glucocorticoid receptor in mineralocorticoid/salt mediated cardiac fibrosis. Endocrinology. 147:5901-6. IF=4.993 Citations:41
  13. Wong, S., Brennan, F.E., Young, M.J., Fuller, P.J. and T.J. Cole (2007). A Direct Effect of Aldosterone on Endothelin-1 Gene Expression in vivo. Endocrinology. 148:1511-7. IF=4.993 Citations: 54
  14. Rickard, A.J., Morgan, J., Funder, JW., Fuller, PJ., and M.J. Young (2007). Does glucocorticoid receptor blockade exacerbate tissue damage following mineralocorticoid/salt administration? Endocrinology. 148:4829-4835. IF= 4.993 Citations:26
  15. Clyne CD, Chang CY, Safi R, Fuller PJ, McDonnell DP and M.J. Young (2009). Purification and characterization of recombinant human mineralocorticoid receptor. Mol Cell Endocrinol. 10;302(1):81-5. IF= 4.119 Citations: 19
  16. Wilson, P., Morgan, J., Funder, J.W., Fuller, PJ., and M.J. Young (2009)Mediators of mineralocorticoid receptor-induced profibrotic inflammatory responses in the heart. Clin Sci. 116(9):731-9. IF=4.613 Citations:51
  17. Rickard, A.J., Morgan, J., Tesch, G., Funder, J.W., Fuller, P.J., and M.J. Young  (2009). Deletion of mineralocorticoid receptors from macrophages protects against DOC/salt-induced cardiac fibrosis and hypertension. Hypertension. 54(3):537-43. CI=53 IF=6.8. Citations: 291
  18. Sierens J1, Jakody I, Poobalan Y, Meachem SJ, Knower K, Young MJ, Sirianni R, Pezzi V, and CD Clyne. (2010). Localization and regulation of aromatase liver receptor homologue-1 in the developing rat testis. Mol Cell Endocrinol. 29;323(2):307-13. Citations: 22
  19. Young M.J., Morgan J, Brolin K, et al. (2010). Activation of Mineralocorticoid Receptors by Exogenous Glucocorticoids and the Development of Cardiovascular Inflammatory Responses in Adrenalectomized Rats. Endocrinology. 51(6): 2622-2628 IF= 4.993 Citations:28
  20. Yang J, Chang CY, Safi R, Morgan J, McDonnell DP, Fuller PJ, Clyne CD, Young MJ. (2011). Identification of ligand-selective peptide antagonists of the mineralocorticoid receptor using phage display. Mol Endocrinol. 25(1):32-43. IF= 4.889 Citations:51
  21. Mellor KM, Bell JR, Young MJ, Ritchie RH, Delbridge LM. (2011). Myocardial autophagy activation and suppressed survival signaling is associated with insulin resistance in fructose-fed mice. J Mol Cell Cardiol. 50(6):1035-43. IF= 5.499 Citations:200
  22. Lim AK, Ma FY, Nikolic-Paterson DJ, Ozols E, Young MJ, Bennett BL, Friedman GC, Tesch GH (2011). Evaluation of JNK Blockade as an Early Intervention Treatment for Type 1 Diabetic Nephropathy in Hypertensive Rats. Am J Nephrol. 26;34(4):337-346. IF= 2.658 Citations: 43
  23. Bienvenu, LA., Morgan J., Tesch, G.H., Cranston, G.A., Fletcher, EK., Delbridge, LM, MJ. Young (2012). Macrophage mineralocorticoid receptor signaling plays a key role in aldosterone-independent cardiac fibrosis. Endocrinology. 153(7):3416-25. IF=4.993 Citations:109
  24. Rickard, AJ, Morgan, J., Bienvenu, LA., Fletcher, EK., Cranston, GA, Shen, JZ., Reichelt, ME., Delbridge, L.M. and M.J. Young (2012). Cardiomyocyte MR signaling is essential for DOC/salt-mediated cardiac fibrosis and blood pressure regulation. Hypertension. 60:1443-50. IF=6.8. Citations:96
  25. Rickard, A.J., Morgan, J., Chrissobolis, S., Miller, A.A., Sobey, C.G. and M.J. Young. (2014). Endothelial cell mineralocorticoid receptors regulate DOC/salt-mediated cardiac remodeling and vascular reactivity, but not blood pressure. Hypertension 63(5):1033-40. Selected for Editorial Comment IF=6.8. Citations:119
  26. Shen, J.Z., Morgan, J., Tesch, G.H., Fuller, P.J. and Young, M.J. (2014) CCL2-dependent macrophage recruitment is critical for mineralocorticoid receptor-mediated cardiac fibrosis, inflammation, and blood pressure responses in male mice. Endocrinology. 155(3):1057-66. Citations:51
  27. Huang LL, Nikolic-Paterson DJ, Han Y, Ozols E, Ma F, Young MJ, Tesch GH. (2014) Myeloid mineralocorticoid receptor activation contributes to progressive kidney disease. J Am Soc Nephrol. 2014 Oct;25(10):2231-40. Citations: 23
  28. Lazarus, K.A., Brown, K.A., Young, M.J., Zhao, Z., Coulson, R., Chand, A.L. and C.D. Clyne (2014). Conditional over-expression of Liver Receptor Homolog -1 in female mouse mammary epithelium results in altered mammary morphogenesis via the induction of TGF-b. Endocrinology, 155(5):1606-17. Citations: 13
  29. Armani, A., Cinti, F., Marzolla, V., Morgan, J., Cranston,G.A.,Antelmi, A., Carpinelli, G., Canese, R., Pagotto, U., Quarta, C.,Malorni, W., Matarrese, P., Marconi, M., Fabbri, A., Rosano, G., Cinti, S., Young, M.J. (equal last author) and M. Caprio.(2014). Mineralocorticoid Receptor antagonism counters metabolic dysfunctions induced by high fat diet in mice, through browning of the adipose organ. FASEB J. 28(8):3745-57. Citations: 135 
  30. Rogerson, F., Yao, Y., Young M.J. and P.J. Fuller (2014). Identification and characterization of a ligand selective mineralocorticoid receptor coactivator. FASEB J. 2014 Oct;28(10):4200-10 Citations:28
  31. Yang, J., Fuller, P.J., Shibata, H., Morgan, J., McDonnell,D.M., Clyne, C.D. and M.J. Young. (2014) Use of phage display to identify novel mineralocorticoid receptor-interacting proteins. Molecular Endocrinology. 28(9):1571-84. Citations: 29
  32. J. Yang, P.J. Fuller, J. Morgan, H. Shibata, C.D. Clyne, and M.J. Young. (2015) Gemin4 functions as a cell- and gene-specific corepressor of the mineralocorticoid receptor. Journal of Molecular Endocrinology. 54(2):149-60. Citations: 17
  33. T.J. Cole, L. Terella, J. Morgan, M. Alexiadis, P. Enriori, M.J. Young, and P.J. Fuller (2015). Aldosterone-mediated renal sodium transport requires intact mineralocorticoid receptor DNA-binding in the mouse. Endocrinology. 156(8):2958-68. Citations:9
  34. L.A. Bienvenu, M.E. Reichelt, J. Morgan,E.K. Fletcher, J.R. Bell, A.J. Rickard, L.M. Delbridge and M.J. Young (2015). Cardiomyocyte mineralocorticoid receptor activation impairs acute cardiac functional recovery after ischemic insult. Hypertension. 66(5):970-7. Citations: 16
  35. A. Winship., K. Koga, E. Menkhorst, M. Van Sinderen, K. Rainczuk, M. Nagai, C. Cuman, J.Yap, JG Zhang, D. Simmons, M.J. Young and E. Dimitriadis (2015)  Interleukin-11 alters placentation and causes preeclampsia features in mice. Proc Natl Acad Sci U S A. 29;112(52):15928-33. Citations:64
  36. Q.N. Dinh, M.J. Young, G.R. Drummond, C.G. Sobey, S. Chrissobolis. (2016) Aldosterone-induced oxidative stress and inflammation in the brain are mediated by the endothelial cell mineralocorticoid receptor. Journal of Hypertension. 1637:146-53. Citations: 68
  37. Nagase, M., Kurihara, H., Aiba, A., Young M.J. and T. Sakai. (2016) Deletion of Rac1GTPase in the Myeloid Lineage Protects against Inflammation-Mediated Kidney Injury in Mice. PLOS Mar 3;11(3):e0150886. Citations: 19
  38. J.Z. Shen, J Morgan, G.H. Tesch, A.J. Rickard, S Chrissobolis, G.R. Drummond, P.J. Fuller, M.J. Young. (2016) Myeloid mineralocorticoid receptor signalling determines tissue macrophage regulation of cardiovascular inflammation and remodelling in male mice. Endocrinology Aug;157(8):3213-23. Citations 56
  39. L.A. Bienvenu, J. Morgan, L.M.D. Delbridge and M.J. Young. (2017) Chronic nitric oxide deficiency impairs acute cardiac functional recovery after ischemia in female mice; protective effects of cardiomyocyte mineralocorticoid receptor knockout. Journal of Molecular and Cellular Cardiology 30;112:8-15. Citations:15
  40. E.K. Fletcher, J. Morgan, D. Kennaway, L.M.D Delbridge, P.J. Fuller, C.D. Clyne and M.J. Young. (2017) DOC/salt mediated cardiac inflammation and fibrosis requires a functional circadian clock in male mice. Endocrinology. 1;158(9):2906-2917 Citations:15
  41. C.B. Magne Nde, G.C. Gimeno; M. Docanto, K.C  Knower,  M.J. Young, J. Buehn, E. Sayed and  C.D.  Clyne (2018). Timeless is a novel Estrogen Receptor co-activator involved in multiple signalling pathways in MCF-7 cells. Journal of Molecular Biology. 430(10):1531-1543. Citations:14
  42. M.P Bonham, G. Leung, R. Davis, T.L Sletten, Murgia, C., M.J. Young, Eikelis, N., Lambert, E.A., C.E Huggins. (2018) Does modifying the timing of meal intake improve cardiovascular risk factors? A pilot intervention in night shift workers with abdominal obesity. British Medical Journal Open. 8(3):e020396 Citations:14
  43. E.K. Fletcher, M. Kanki, J. Morgan1, D.W. Ray, L.M. Delbridge, P.J. Fuller, C.D. Clyne, M.J. Young. (2019) Cardiomyocyte transcription is controlled by combined MR and circadian clock signalling. Journal of Endocrinology 241 (1); 17-29. Citations:14
  44. C.B. Bui, M. Kolodziej, E. Lamanna, K. Elgass, A. Sehgal, I Rudloff, D.O. Schwenke, H. Tsuchimochi, M. Kroon, S.X. Cho, A. Maksimenko, M. Cholewa, P.J. Berger, M.J.Young, J. Bourke, J.T. Pearson, M.F. Nold, C.A. Nold. (2019) Interleukin-1 receptor antagonist protects newborn mice against pulmonary hypertension. Frontiers in Immunology, section Cytokines and Soluble Mediators in Immunity. 10: 1480 Citations: 26
  45. P.J. Fuller, R. Jin, YZ Yao, B. Martín-Fernández, M.J. Young, S. He, B.J. Smith.(2019). Molecular Evolution of the Switch for Progesterone from Mineralocorticoid Receptor Agonist to Antagonist. Proceedings National Academy of Science. 116(37)18578-18583 Citations: 25
  46. Yin, L., Gwini, SM., Shen, JSZ., Libianto, R., Young, MJ., Fuller, P.J. and J. Yang. (2020) Impact of Victoria’s first dedicated Endocrine Hypertension Service on the pattern of primary aldosteronism diagnoses. Medical Journal of Australia. 51(8):1255-1261
  47. P. Solanki, S.M. Gwini, P.J. Fuller, J. Shen, James C.G. Doery, M.J. Young, K.W. Choy, J. Yang. Age and sex-specific reference ranges are needed for the Aldosterone/Renin Ratio, Clinical Endocrinology. 93(3):221-228 Citations : 10
  48. J. Cohen, R. Bellomo, L. Billot, L. Burrell, D. Evans, S. Finfer, N. Hammond, Q. Li, D. Liu, C. McArthur, B. McWhinney, John Moore, J. Myburgh, S. Peake, C. Pretorius, D., Rajbhandari,A., Rhodes, M. Saxena,J. Ungerer, M.J, Young & B. Venkatesh (2020). The relationship between cortisol, aldosterone, ascorbic acid and adrenocortical gene expression with clinical outcomes in patients treated with hydrocortisone for septic shock. American Journal of Respiratory and Critical Care Medicine. 202(5):700-707. Citations : 6
  49. G.S.Z. Ong, J. Morgan, D. Saville, A. Mansell, J.K. Dowling, G.H. Tesch, P.J. Fuller, M.J. Young (2020). Mineralocorticoid Receptor-dependent pathways regulate the macrophage response to proinflammatory stimuli and promote cardiac tissue inflammation. Journal of Endocrinology. 246(2):123-134. Citations : 5
  50. R. Hu,X. Li, C. Peng, R. Gao, L. Ma, J. Hu, T. Luo, H. Qing, Y. Wang, Q. Ge, Z. Wang, C. Wu, X. Xiao, J. Yang, M.J. Young, Q. Li, S. Yang (2020). miR-196b-5p-enriched Extracellular Vesicles from Tubular Epithelial Cells Mediated Aldosterone-induced Renal Fibrosis in Diabetic Mice. BMJ Diabetes Open Diabetes Research and Care. 8(1):e001101.
  51. E. Menkhorst, W. Zhou, L. Santos, S. Delforce, T. So, K. Rainczuk, H. Loke, A. Syngelaki, S. Varshney, N. Williamson, K. Pringle, M.J. Young, K. Nicolaides, Y. St-Pierre and E. Dimitriadis. (2020) Galectin-7 impairs placentation and causes preeclampsia features in mice. Hypertension. 76(4):1185-1194 Citations : 13
  52. T. B. Doan, V. Cheung, C.D. Clyne2, H.N. Hilton, N. Eriksson, M.J. Young, J.W. Funder, G.E.O. Muscat, P.J. Fuller, C.L. Clarke, J.D. Graham (2020). A tumour suppressive relationship between mineralocorticoid and retinoic acid receptors activates a transcriptional program consistent with a reverse Warburg effect in breast cancer. Breast Cancer Research. 22(1):122 Citations : 7
  53. R. Libianto, J. Hu, M.R. Chee, J. Hoo, Y.Y. Lim, J.Z. Shen, Q. Li, M.J. Young, P.J. Fuller, J. Yang. (2020) A multi-centre study of neutrophil-to-lymphocyte ratio in primary aldosteronism. Journal of the Endocrine Society. 4(12):bvaa153
  54. Chee NYN, Abdul-Wahab A, Libianto R, Gwini SM, Doery JCG, Choy KW, Chong W, Lau KK, Lam Q, MacIsaac RJ, Chiang C, Shen J, Young M.J., Fuller PJ, Yang J. (2020). Utility of adrenocorticotropic hormone in adrenal vein sampling despite the occurrence of discordant lateralization. Clin Endocrinol. 93(4):394-403.
  55. Burke SL, Barzel B, Jackson KL, Gueguen C, Young MJ, Head GA. (2021). Role of Mineralocorticoid and Angiotensin Type 1 Receptors in the Paraventricular Nucleus in Angiotensin-Induced Hypertension. Front Physiol. 2021 Mar 8;12:640373.
  56. R. Libianto, S. Menzes, O. Narayan, J. Cameron, P.J. Fuller, J. Yang and M.J. Young (2021). Comparison of ambulatory blood pressure between patients with primary aldosteronism and other forms of hypertension. Clinical Endocrinology 94(3):353-360. Citations : 3
  57. E. Barros, J.P. Rigalli, A. Tapia-Castillo, A. Vecchiola, M.J. Young, J. Heenderop, R. Bindels, C. E. Fardella, C. A. Carvajal. (2021) Proteomic Profile of Urinary Extracellular Vesicles Identifies AGP1 as a Potential Biomarker of Primary Aldosteronism. Endocrinology, Volume 162 (4). Citations : 4
  58. Min Ru Chee, Jesse Hoo, Renata Libianto, Stella Gwini, Garun Hamilton, Om Narayan, Morag J Young, Peter Fuller, and Jun Yang (2021). Prospective Screening for Primary Aldosteronism in Patients with Suspected Obstructive Sleep Apnea. Hypertension. 77(6):2094-2103. Citations : 6
  59. Jun Yang, Stella May Gwini, Lawrence J Beilin, Markus Schlaich, Michael Stowasser, Morag J Young, Peter J Fuller, and Trevor A Mori.(2021)Relationship between the aldosterone-to-renin ratio and blood pressure in young adults: a longitudinal study.  Hypertension. 78(2):387-396. Citations : 3
  60. Yin Yu Lim, Renata Libianto, Jimmy Shen, Morag J. Young, Peter J. Fuller and Jun Yang (2021).  Impact of Victoria’s first dedicated endocrine hypertension service on the pattern of primary aldosteronism diagnoses. Internal Medical Journal. 51; 1255–1261. Citations : 7
  61. Lao, J.C., Bui, CB., Pang, MA., Cho, S.X., Rudloff, I., Sehgal, A., Elgass, K., Pearson, J., Mangan, NE., Maksimenko, A., Starkey, MR., Hansbro, PM., Camden Y. Lo, CY., Skuza, EM Young, M.J., Beker, F., Collins, C., Kamlin, O., König, K., Malhotra, A., Tan, K., Theda, C., Veldman, A., Berger, PJ., Nold-Petry, CA Marcel F. Nold,MF. (2022). Immune Polarization in Preterm Infants and its Impact on Cardiopulmonary Disease. Science and Translational Medicine. 14(639):eaaz8454
  62. Renata Libianto, Grant M Russell, Michael Stowasser, Stella M Gwini, Peta Nuttall, Jimmy Shen, Morag J Young, Peter J Fuller, Jun Yang (2022) Detecting primary aldosteronism in Australian primary care: a prospective study The medical Journal of Australia. https://onlinelibrary.wiley.com/doi/full/10.5694/mja2.51438
  63. E. Menkhorst, W. Zhou, L. Santos, S. Delforce, T. So, K. Rainczuk, H. Loke, A. Syngelaki, S. Varshney, N. Williamson, K. Pringle, M.J. Young, K. Nicolaides, Y. St-Pierre and E. Dimitriadis. Galectin-7 dysregulates renin-angiotensin-aldosterone and NADPH oxide synthase pathways in preeclampsia (2022). Pregnancy Hypertension. 30:130-136
  64. Colin D. Clyne, Alexander Cowcher, Kevin Kusnadi, James Morgan, Jun Yang, Peter J. Fuller, Morag J. Young (2022). Regulation of the mineralocorticoid receptor transactivation by circadian protein timeless. Journal of Molecular Endocrinology. JME-21-0279 online

Research Projects

For project inquiries, contact our research group head.

School Research Themes

Cardiometabolic

Key Contact

For further information about this research, please contact Head of Laboratory Assoc Professor Morag Young

Department / Centre

Baker Department of Cardiometabolic Health

Unit / Centre

Cardiovascular Endocrinology Group

MDHS Research library
Explore by researcher, school, project or topic.