Involvement of Mitochondrial Permeability Transition, Glutathione Status, Pentose Phosphate Pathway and Oxidative Damage in the Protective Effect of Fasting on the Ischaemic‐reperfused Rat Heart

Prendes, María Gabriela Marina; González, Marcela; Torresin, M. E.; Hermann, R; Pascale, Natalia G; Jaitovich, María del Mar; Savino, E.; Varela, A

doi:10.1111/j.1440-1681.2008.05122.x

Cited by 9 publications

(4 citation statements)

References 45 publications

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“…Though prolonged caloric limitation is a well-established protective stimulus, effects of brief or moderate fasting await detailed study in DM animals. Severe CR for 11 days generates unique I–R tolerance [ 490 ], and 24–72 h of fasting enhances cardiac I–R tolerance and mitochondrial viability in non-DM hearts [ 491 , 492 ]. There are surprisingly few studies of caloric limitation in DM.…”

Section: Potential ‘Membrane-targeted’ Therapies?mentioning

confidence: 99%

Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection

Russell

Toit

Peart

et al. 2017

Cardiovasc Diabetol

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Cardiovascular disease, predominantly ischemic heart disease (IHD), is the leading cause of death in diabetes mellitus (DM). In addition to eliciting cardiomyopathy, DM induces a ‘wicked triumvirate’: (i) increasing the risk and incidence of IHD and myocardial ischemia; (ii) decreasing myocardial tolerance to ischemia–reperfusion (I–R) injury; and (iii) inhibiting or eliminating responses to cardioprotective stimuli. Changes in ischemic tolerance and cardioprotective signaling may contribute to substantially higher mortality and morbidity following ischemic insult in DM patients. Among the diverse mechanisms implicated in diabetic impairment of ischemic tolerance and cardioprotection, changes in sarcolemmal makeup may play an overarching role and are considered in detail in the current review. Observations predominantly in animal models reveal DM-dependent changes in membrane lipid composition (cholesterol and triglyceride accumulation, fatty acid saturation vs. reduced desaturation, phospholipid remodeling) that contribute to modulation of caveolar domains, gap junctions and T-tubules. These modifications influence sarcolemmal biophysical properties, receptor and phospholipid signaling, ion channel and transporter functions, contributing to contractile and electrophysiological dysfunction, cardiomyopathy, ischemic intolerance and suppression of protective signaling. A better understanding of these sarcolemmal abnormalities in types I and II DM (T1DM, T2DM) can inform approaches to limiting cardiomyopathy, associated IHD and their consequences. Key knowledge gaps include details of sarcolemmal changes in models of T2DM, temporal patterns of lipid, microdomain and T-tubule changes during disease development, and the precise impacts of these diverse sarcolemmal modifications. Importantly, exercise, dietary, pharmacological and gene approaches have potential for improving sarcolemmal makeup, and thus myocyte function and stress-resistance in this ubiquitous metabolic disorder.

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Section: Potential ‘Membrane-targeted’ Therapies?mentioning

confidence: 99%

Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection

Russell

Toit

Peart

et al. 2017

Cardiovasc Diabetol

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“…KEGG indicated that signaling pathways were enrichment in methylation modification pattern B (Supporting Information: Figure ), including Cytochrome P450, Glutathione Metabolism, Ribosome, Proteasome, Arachidonic Acid Metabolism, Base Excision Repair and Pentose Phosphate Pathway. Since the activation of the seven signaling pathways was associated with DCM risk (Ganapathi et al, 2020; Kanoh et al, 1999; Lei et al, 2009; Lu et al, 2012; Marina Prendes et al, 2009; Spänig et al, 2019; Zhou et al, 2016), it indicated that methylation modification pattern B (but not methylation modification patterns A and C) was more likely linked to the risk of DCM. In addition, the Venn diagram revealed that 501 genes were involved in m6A methylation modification (Supporting Information: Figure ).…”

Section: Resultsmentioning

confidence: 99%

“…RNA modification exists in all living forms, and more than 150 RNA modifications have been identified, including N1-methyladenosine (m1A), 5-methylcytosine (m5C), and N6-methyladenosine (m6A), in which, m6A methylation is the most prevalent RNA modification and is mediated by various m6A regulators (Patil et al, 2016). Since m6A RNA methylation has impact on immunocyte function and disturb antitumor immunity (Han et al, 2019;Ma et al, 2021), we speculate that m6A RNA methylation may involve in the immune microenvironment disorder. This study is to explore the role and mechanisms of m6A-related immune microenvironment disorder in the development of DCM.…”

mentioning

confidence: 99%

m6A regulator‐mediated RNA methylation modification remodels immune microenvironment in dilated cardiomyopathy

Wang

Cheng

Wang

2023

Journal Cellular Physiology

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The latest evidence suggested that the onset of dilated cardiomyopathy (DCM) is closely associated with immune microenvironment disturbance. Since N6‐methyladenosine (m6A) RNA methylation impacts on immunocyte function and antitumor immunity, it is predictable that m6A RNA methylation may result in immune microenvironment disorder. Here, we attempted to verify this hypothesis. We used single‐sample gene set enrichment analysis (ssGSEA) to investigate the infiltration abundance of immunocytes, single‐cell RNA‐Seq to identify key m6A regulator, and a doxorubicin (Dox)‐induced DCM mouse model to confirm our findings. ssGSEA revealed a higher infiltration abundance of CD8+ T lymphocytes, NK cells, monocytes, and B+ lymphocytes in DCM myocardium tissue. Single‐cell RNA‐Seq indicated a critical role of IGFBP2 in DCM. Cross‐checking analysis hinted an interaction between IGFBP2 and NSUN5, ALYREF, RRP8, and ALKBH3. Mechanically, IGFBP2‐mediated RNA methylation deteriorated the immune microenvironment and thus increased the risk of DCM by enhancing CD8+ T lymphocyte, NK cell, monocyte, B+ lymphocyte infiltration and activating check‐point, MHC‐I, and T cell co‐stimulation signaling pathways. In the DCM mouse model, echocardiography indicated a significant reduction in ejection fraction (EF) and fractional shortening (FS) and an increase in left ventricular internal dimensions at systole (LVIDs) and diastole (LVIDd). MASSON staining indicated an increased fibrosis in myocardium tissue. qPCR and immunofluorescence staining indicated a significant increase in mRNA and protein levels of IGFBP2. The present study indicated that IGFBP2‐mediated RNA methylation remodeled the immune microenvironment and increased the risk of DCM. IGFBP2 may serve as potential therapeutic target for DCM.

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“…In addition to these insights, the ability of caloric restriction or fasting to protect against IR-induced injury is associated with decreased MPTP opening and increased respiratory function, increased activity of NADPH-generating glucose-6-phosphate dehydrogenase (G6PDH) and attendant increases in GSH/GSSG redox, and decreased biomarkers of oxidant stress [35,164,316] (Figure 7). It is interesting that short-term fasting has been found to confer similar protection against IRI as more long-term caloric restriction [35,440,532], as does chronic, but intermittent fasting [229].…”

Section: Caloric Restrictionmentioning

confidence: 99%

Cell Survival Programs and Ischemia /Reperfusion: Hormesis, Preconditioning, and Cardioprotection

Krenz¹,

Baines²,

Kalogeris³

et al. 2013

Colloquium Series on Integrated Systems Physiology: From Molecule to Function

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ii This e-book is an original work commissioned for the Colloquium Digital Library of Life Sciences, a curated collection of time-saving pedagogical resources for researchers and students who want to quickly get up to speed in a new area of life science/biomedical research. Each e-book available in Colloquium is an in-depth overview of a fast-moving or fundamental area of research, authored by a prominent contributor to the field. We call these resources 'Lectures' because authors are asked to provide an authoritative, state-of-the-art overview of their area of expertise, in a manner that is accessible to a broad, diverse audience of scientists (similar to a plenary or keynote lecture at a symposium/meeting/colloquium). Readers are invited to keep current with advances in various disciplines, gain insight into fields other than their own, and refresh their understanding of core concepts in cell & molecular biology. Physiology is a scientific discipline devoted to understanding the functions of the body. It addresses function at multiple levels, including molecular, cellular, organ, and system. An appreciation of the processes that occur at each level is necessary to understand function in health and the dysfunction associated with disease. Homeostasis and integration are fundamental principles of physiology that account for the relative constancy of organ processes and bodily function even in the face of substantial environmental changes. This constancy results from integrative, cooperative interactions of chemical and electrical signaling processes within and between cells, organs and systems. This eBook series on the broad field of physiology covers the major organ systems from an integrative perspective that addresses the molecular and cellular processes that contribute to homeostasis. Material on pathophysiology is also included throughout the eBooks. The state-of the-art treatises were produced by leading experts in the field of physiology. Each eBook includes stand-alone information and is intended to be of value to students, scientists, and clinicians in the biomedical sciences. Since physiological concepts are an ever-changing work-in-progress, each contributor will have the opportunity to make periodic updates of the covered material.Published titles (for future titles please see the website, www.morganclaypool.com/page/lifesci) ABSTRACTThe major purpose of this book is to review the evidence supporting the concept that intrinsic cell survival programs can be activated by a variety of mildly noxious stimuli or pharmacologic agents to confer protection against the deleterious effects of ischemia/reperfusion (I/R). We begin with a discussion of the concept of hormesis (a term used most extensively in the toxicologic literature which refers to biphasic cellular responses that depend on concentration or intensity of a stimulus), review the seminal studies that led to the discovery of the cardioprotective effects of ischemic preconditioning, and outline its therapeutic potential (Chapter 1). This is followed ...

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Involvement of Mitochondrial Permeability Transition, Glutathione Status, Pentose Phosphate Pathway and Oxidative Damage in the Protective Effect of Fasting on the Ischaemic‐reperfused Rat Heart

Cited by 9 publications

References 45 publications

Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection

Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection

m6A regulator‐mediated RNA methylation modification remodels immune microenvironment in dilated cardiomyopathy

Cell Survival Programs and Ischemia /Reperfusion: Hormesis, Preconditioning, and Cardioprotection

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