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Article ; Online: The cardiomyocyte origins of diastolic dysfunction: cellular components of myocardial "stiffness".

Janssens, Johannes V / Raaijmakers, Antonia J A / Weeks, Kate L / Bell, James R / Mellor, Kimberley M / Curl, Claire L / Delbridge, Lea M D

American journal of physiology. Heart and circulatory physiology

2024 Volume 326, Issue 3, Page(s) H584–H598

Abstract: The impaired ability of the heart to relax and stretch to accommodate venous return is generally understood to represent a state of "diastolic dysfunction" and often described using the all-purpose noun "stiffness." Despite the now common qualitative ... ...

Abstract	The impaired ability of the heart to relax and stretch to accommodate venous return is generally understood to represent a state of "diastolic dysfunction" and often described using the all-purpose noun "stiffness." Despite the now common qualitative usage of this term in fields of cardiac patho/physiology, the specific quantitative concept of stiffness as a molecular and biophysical entity with real practical interpretation in healthy and diseased hearts is sometimes obscure. The focus of this review is to characterize the concept of cardiomyocyte stiffness and to develop interpretation of "stiffness" attributes at the cellular and molecular levels. Here, we consider "stiffness"-related terminology interpretation and make links between cardiomyocyte stiffness and aspects of functional and structural cardiac performance. We discuss cross bridge-derived stiffness sources, considering the contributions of diastolic myofilament activation and impaired relaxation. This includes commentary relating to the role of cardiomyocyte Ca
MeSH term(s)	Humans ; Myocytes, Cardiac/physiology ; Myocardium ; Cardiomyopathies ; Myofibrils ; Diastole/physiology ; Myosins ; Connectin
Chemical Substances	Myosins (EC 3.6.4.1) ; Connectin
Language	English
Publishing date	2024-01-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00334.2023
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Article: New Perspectives on Sex Steroid and Mineralocorticoid Receptor Signaling in Cardiac Ischemic Injury.

Bienvenu, Laura A / Bell, James R / Weeks, Kate L / Delbridge, Lea M D / Young, Morag J

Frontiers in physiology

2022 Volume 13, Page(s) 896425

Abstract: The global burden of ischemic heart disease is burgeoning for both men and women. Although advances have been made, the need for new sex-specific therapies targeting key differences in cardiovascular disease outcomes in men and women remains. ... ...

Abstract	The global burden of ischemic heart disease is burgeoning for both men and women. Although advances have been made, the need for new sex-specific therapies targeting key differences in cardiovascular disease outcomes in men and women remains. Mineralocorticoid receptor directed treatments have been successfully used for blood pressure control and heart failure management and represent a potentially valuable therapeutic option for ischemic cardiac events. Clinical and experimental data indicate that mineralocorticoid excess or inappropriate mineralocorticoid receptor (MR) activation exacerbates ischemic damage, and many of the intracellular response pathways activated in ischemia and subsequent reperfusion are regulated by MR. In experimental contexts, where MR are abrogated genetically or mineralocorticoid signaling is suppressed pharmacologically, ischemic injury is alleviated, and reperfusion recovery is enhanced. In the chronic setting, mineralocorticoid signaling induces fibrosis, oxidative stress, and inflammation, which can predispose to ischemic events and exacerbate post-myocardial infarct pathologies. Whilst a range of cardiac cell types are involved in mineralocorticoid-mediated regulation of cardiac function, cardiomyocyte-specific MR signaling pathways are key. Selective inhibition of cardiomyocyte MR signaling improves electromechanical resilience during ischemia and enhances contractile recovery in reperfusion. Emerging evidence suggests that the MR also contribute to sex-specific aspects of ischemic vulnerability. Indeed, MR interactions with sex steroid receptors may differentially regulate myocardial nitric oxide bioavailability in males and females, potentially determining sex-specific post-ischemic outcomes. There is hence considerable impetus for exploration of MR directed, cell specific therapies for both women and men in order to improve ischemic heart disease outcomes.
Language	English
Publishing date	2022-06-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2022.896425
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Article ; Online: The big picture: cardiac sex-age interactions and proteogenomic insights.

Janssens, Johannes V / Bell, James R / Weeks, Kate L / Mellor, Kimberley M / Delbridge, Lea M D

American journal of physiology. Heart and circulatory physiology

2022 Volume 323, Issue 4, Page(s) H640–H642

MeSH term(s)	Proteogenomics ; Proteome/genetics ; Proteomics
Chemical Substances	Proteome
Language	English
Publishing date	2022-09-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00418.2022
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Article ; Online: Cellular Mechanisms Mediating Exercise-Induced Protection against Cardiotoxic Anthracycline Cancer Therapy.

Dozic, Sanela / Howden, Erin J / Bell, James R / Mellor, Kimberley M / Delbridge, Lea M D / Weeks, Kate L

Cells

2023 Volume 12, Issue 9

Abstract: Anthracyclines such as doxorubicin are widely used chemotherapy drugs. A common side effect of anthracycline therapy is cardiotoxicity, which can compromise heart function and lead to dilated cardiomyopathy and heart failure. Dexrazoxane and heart ... ...

Abstract	Anthracyclines such as doxorubicin are widely used chemotherapy drugs. A common side effect of anthracycline therapy is cardiotoxicity, which can compromise heart function and lead to dilated cardiomyopathy and heart failure. Dexrazoxane and heart failure medications (i.e., beta blockers and drugs targeting the renin-angiotensin system) are prescribed for the primary prevention of cancer therapy-related cardiotoxicity and for the management of cardiac dysfunction and symptoms if they arise during chemotherapy. However, there is a clear need for new therapies to combat the cardiotoxic effects of cancer drugs. Exercise is a cardioprotective stimulus that has recently been shown to improve heart function and prevent functional disability in breast cancer patients undergoing anthracycline chemotherapy. Evidence from preclinical studies supports the use of exercise training to prevent or attenuate the damaging effects of anthracyclines on the cardiovascular system. In this review, we summarise findings from experimental models which provide insight into cellular mechanisms by which exercise may protect the heart from anthracycline-mediated damage, and identify knowledge gaps that require further investigation. Improved understanding of the mechanisms by which exercise protects the heart from anthracyclines may lead to the development of novel therapies to treat cancer therapy-related cardiotoxicity.
MeSH term(s)	Humans ; Cardiotoxicity/etiology ; Cardiotoxicity/prevention & control ; Cardiotoxicity/drug therapy ; Anthracyclines/adverse effects ; Antibiotics, Antineoplastic/therapeutic use ; Antineoplastic Agents/adverse effects ; Heart Failure/drug therapy ; Topoisomerase II Inhibitors ; Neoplasms/drug therapy
Chemical Substances	Anthracyclines ; Antibiotics, Antineoplastic ; Antineoplastic Agents ; Topoisomerase II Inhibitors
Language	English
Publishing date	2023-05-04
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12091312
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Article ; Online: Mitochondrial Assays Using Cardiac Stem Cells.

Rosdah, Ayeshah A / Delbridge, Lea M D / Lim, Shiang Y

Methods in molecular biology (Clifton, N.J.)

2019 Volume 2029, Page(s) 175–183

Abstract: Ischemic heart disease is the leading cause of death worldwide. Stem cell therapy to repair and regenerate the infarcted myocardium is a promising approach to address this unmet medical need. However, the poor survival of transplanted cells in the ... ...

Abstract	Ischemic heart disease is the leading cause of death worldwide. Stem cell therapy to repair and regenerate the infarcted myocardium is a promising approach to address this unmet medical need. However, the poor survival of transplanted cells in the hostile ischemic myocardium has been a major hurdle in achieving an effective cell therapy against myocardial infarction. As such, novel strategies to promote the survival of transplanted cells are highly sought after. Mitochondria are intimately involved in cell survival and have been the main organelles being targeted for cytoprotection. Mitochondrial morphology is linked to mitochondrial function and cell viability. Therefore, quantitative methodologies to obtain reliable and reproducible results of mitochondrial morphology and function are essential for identifying and developing new cytoprotective strategies to enhance the survival of stem cells post-transplantation. Here, we describe methods for assessing mitochondrial morphology, mitochondrial membrane potential, and mitochondrial reactive oxygen species production.
MeSH term(s)	Cell Survival/physiology ; Cytoprotection/physiology ; Humans ; Membrane Potential, Mitochondrial/physiology ; Mitochondria/metabolism ; Mitochondria/physiology ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardial Ischemia/metabolism ; Myocardial Ischemia/pathology ; Myocardium/metabolism ; Myocardium/pathology ; Reactive Oxygen Species/metabolism ; Regeneration/physiology ; Stem Cell Transplantation/methods ; Stem Cells/cytology ; Stem Cells/metabolism
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2019-07-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-9631-5_14
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: HFpEF-Time to Explore the Role of Genetic Heterogeneity in Phenotypic Variability: New Mechanistic Insights Offer Promise for Personalized Therapies.

Porrello, Enzo R / Delbridge, Lea M D

Circulation

2019 Volume 140, Issue 20, Page(s) 1607–1609

MeSH term(s)	Animals ; Clinical Decision-Making ; Gene-Environment Interaction ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Heart Failure/diagnosis ; Heart Failure/genetics ; Heart Failure/physiopathology ; Heart Failure/therapy ; Humans ; Multifactorial Inheritance ; Phenotype ; Precision Medicine ; Prognosis ; Risk Factors ; Stroke Volume/genetics ; Ventricular Function, Left/genetics
Language	English
Publishing date	2019-11-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIRCULATIONAHA.119.042496
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Article: Mechanical loading reveals an intrinsic cardiomyocyte stiffness contribution to diastolic dysfunction in murine cardiometabolic disease.

Janssens, Johannes V / Raaijmakers, Antonia J A / Koutsifeli, Parisa / Weeks, Kate L / Bell, James R / Van Eyk, Jennifer E / Curl, Claire L / Mellor, Kimberley M / Delbridge, Lea M D

bioRxiv : the preprint server for biology

2024

Abstract: Cardiometabolic syndromes including diabetes and obesity are associated with occurrence of heart failure with diastolic dysfunction. There are no specific treatments for diastolic dysfunction and therapies to manage symptoms have limited efficacy. ... ...

Abstract	Cardiometabolic syndromes including diabetes and obesity are associated with occurrence of heart failure with diastolic dysfunction. There are no specific treatments for diastolic dysfunction and therapies to manage symptoms have limited efficacy. Understanding of the cardiomyocyte origins of diastolic dysfunction is an important priority to identify new therapeutics. The investigative goal was to experimentally define Key points: Understanding cardiomyocyte stiffness components is an important priority for identifying new therapeutics for diastolic dysfunction, a key feature of cardiometabolic disease. In this study cardiac function was measured
Language	English
Publishing date	2024-04-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.21.581448
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Article ; Online: Protein phosphatase 2A in the healthy and failing heart: New insights and therapeutic opportunities.

Sergienko, Nicola M / Donner, Daniel G / Delbridge, Lea M D / McMullen, Julie R / Weeks, Kate L

Cellular signalling

2021 Volume 91, Page(s) 110213

Abstract: Protein phosphatases have emerged as critical regulators of phosphoprotein homeostasis in settings of health and disease. Protein phosphatase 2A (PP2A) encompasses a large subfamily of enzymes that remove phosphate groups from serine/threonine residues ... ...

Abstract	Protein phosphatases have emerged as critical regulators of phosphoprotein homeostasis in settings of health and disease. Protein phosphatase 2A (PP2A) encompasses a large subfamily of enzymes that remove phosphate groups from serine/threonine residues within phosphoproteins. The heterogeneity in PP2A structure, which arises from the grouping of different catalytic, scaffolding and regulatory subunit isoforms, creates distinct populations of catalytically active enzymes (i.e. holoenzymes) that localise to different parts of the cell. This structural complexity, combined with other regulatory mechanisms, such as interaction of PP2A heterotrimers with accessory proteins and post-translational modification of the catalytic and/or regulatory subunits, enables PP2A holoenzymes to target phosphoprotein substrates in a highly specific manner. In this review, we summarise the roles of PP2A in cardiac physiology and disease. PP2A modulates numerous processes that are vital for heart function including calcium handling, contractility, β-adrenergic signalling, metabolism and transcription. Dysregulation of PP2A has been observed in human cardiac disease settings, including heart failure and atrial fibrillation. Efforts are underway, particularly in the cancer field, to develop therapeutics targeting PP2A activity. The development of small molecule activators of PP2A (SMAPs) and other compounds that selectively target specific PP2A holoenzymes (e.g. PP2A/B56α and PP2A/B56ε) will improve understanding of the function of different PP2A species in the heart, and may lead to the development of therapeutics for normalising aberrant protein phosphorylation in settings of cardiac remodelling and dysfunction.
MeSH term(s)	Heart ; Humans ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Phosphatase 2/metabolism ; Protein Processing, Post-Translational
Chemical Substances	Phosphoproteins ; Protein Phosphatase 2 (EC 3.1.3.16)
Language	English
Publishing date	2021-12-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2021.110213
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Article ; Online: Myocardial glycophagy flux dysregulation and glycogen accumulation characterize diabetic cardiomyopathy.

Mellor, Kimberley M / Varma, Upasna / Koutsifeli, Parisa / Daniels, Lorna J / Benson, Victoria L / Annandale, Marco / Li, Xun / Nursalim, Yohanes / Janssens, Johannes V / Weeks, Kate L / Powell, Kim L / O'Brien, Terence J / Katare, Rajesh / Ritchie, Rebecca H / Bell, James R / Gottlieb, Roberta A / Delbridge, Lea M D

Journal of molecular and cellular cardiology

2024 Volume 189, Page(s) 83–89

Abstract: Diabetic heart disease morbidity and mortality is escalating. No specific therapeutics exist and mechanistic understanding of diabetic cardiomyopathy etiology is lacking. While lipid accumulation is a recognized cardiomyocyte phenotype of diabetes, less ... ...

Abstract	Diabetic heart disease morbidity and mortality is escalating. No specific therapeutics exist and mechanistic understanding of diabetic cardiomyopathy etiology is lacking. While lipid accumulation is a recognized cardiomyocyte phenotype of diabetes, less is known about glycolytic fuel handling and storage. Based on in vitro studies, we postulated the operation of an autophagy pathway in the myocardium specific for glycogen homeostasis - glycophagy. Here we visualize occurrence of cardiac glycophagy and show that the diabetic myocardium is characterized by marked glycogen elevation and altered cardiomyocyte glycogen localization. We establish that cardiac glycophagy flux is disturbed in diabetes. Glycophagy may represent a potential therapeutic target for alleviating the myocardial impacts of metabolic disruption in diabetic heart disease.
MeSH term(s)	Humans ; Diabetic Cardiomyopathies/drug therapy ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Glycogen/metabolism ; Autophagy ; Diabetes Mellitus/metabolism
Chemical Substances	Glycogen (9005-79-2)
Language	English
Publishing date	2024-03-13
Publishing country	England
Document type	Journal Article
ZDB-ID	80157-4
ISSN	1095-8584 ; 0022-2828
ISSN (online)	1095-8584
ISSN	0022-2828
DOI	10.1016/j.yjmcc.2024.02.009
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Article ; Online: Localized cardiomyocyte lipid accumulation is associated with slowed epicardial conduction in rats.

Wells, Simon P / Raaijmakers, Antonia J A / Curl, Claire L / O'Shea, Christopher / Hayes, Sarah / Mellor, Kimberley M / Kalman, Jonathan M / Kirchhof, Paulus / Pavlovic, Davor / Delbridge, Lea M D / Bell, James R

The Journal of general physiology

2023 Volume 155, Issue 11

Abstract: Transmural action potential duration differences and transmural conduction gradients aid the synchronization of left ventricular repolarization, reducing vulnerability to transmural reentry and arrhythmias. A high-fat diet and the associated accumulation ...

Abstract	Transmural action potential duration differences and transmural conduction gradients aid the synchronization of left ventricular repolarization, reducing vulnerability to transmural reentry and arrhythmias. A high-fat diet and the associated accumulation of pericardial adipose tissue are linked with conduction slowing and greater arrhythmia vulnerability. It is predicted that cardiac adiposity may more readily influence epicardial conduction (versus endocardial) and disrupt normal transmural activation/repolarization gradients. The aim of this investigation was to determine whether transmural conduction gradients are modified in a rat model of pericardial adiposity. Adult Sprague-Dawley rats were fed control/high-fat diets for 15 wk. Left ventricular 300 µm tangential slices were generated from the endocardium to the epicardium, and conduction was mapped using microelectrode arrays. Slices were then histologically processed to assess fibrosis and cardiomyocyte lipid status. Conduction velocity was significantly greater in epicardial versus endocardial slices in control rats, supporting the concept of a transmural conduction gradient. High-fat diet feeding increased pericardial adiposity and abolished the transmural conduction gradient. Slowed epicardial conduction in epicardial slices strongly correlated with an increase in cardiomyocyte lipid content, but not fibrosis. The positive transmural conduction gradient reported here represents a physiological property of the ventricular activation sequence that likely protects against reentry. The absence of this gradient, secondary to conduction slowing and cardiomyocyte lipid accumulation, specifically in the epicardium, indicates a novel mechanism by which pericardial adiposity may exacerbate ventricular arrhythmias.
MeSH term(s)	Animals ; Rats ; Myocytes, Cardiac ; Heart Conduction System/physiology ; Rats, Sprague-Dawley ; Arrhythmias, Cardiac ; Lipids ; Action Potentials/physiology
Chemical Substances	Lipids
Language	English
Publishing date	2023-10-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	3118-5
ISSN	1540-7748 ; 0022-1295
ISSN (online)	1540-7748
ISSN	0022-1295
DOI	10.1085/jgp.202213296
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