Epigenetics in Heart Failure: Role of DNA Methylation in Potential Pathways Leading to Heart Failure with Preserved Ejection Fraction

Rabkin, Simon W.; Wong, Chenille N.

doi:10.3390/biomedicines11102815

Biomedicines

2023

DOI: 10.3390/biomedicines11102815

|View full text |Cite

Epigenetics in Heart Failure: Role of DNA Methylation in Potential Pathways Leading to Heart Failure with Preserved Ejection Fraction

Simon W. Rabkin,

Chenille N. Wong

Abstract: This review will focus on epigenetic modifications utilizing the DNA methylation mechanism, which is potentially involved in the pathogenesis of heart failure with preserved ejection fraction (HFpEF). The putative pathways of HFpEF will be discussed, specifically myocardial fibrosis, myocardial inflammation, sarcoplasmic reticulum Ca2+-ATPase, oxidative–nitrosative stress, mitochondrial and metabolic defects, as well as obesity. The relationship of HFpEF to aging and atrial fibrillation will be examined from t… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2024

Publication Types

Select...

Article3

Relationship

Self Cite0

Independent3

Authors

Journals

Cited by 3 publications

References 101 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Exploring the therapeutic potential of tetrahydrobiopterin for heart failure with preserved ejection fraction: A path forward

Xia,

Zhang,

Liu

et al. 2024

Life Sciences

View full text Add to dashboard Cite

Exploring the therapeutic potential of tetrahydrobiopterin for heart failure with preserved ejection fraction: A path forward

Xia,

Zhang,

Liu

et al. 2024

Life Sciences

View full text Add to dashboard Cite

Developmental programming of sarcoplasmic reticulum function improves cardiac anoxia tolerance in turtles

Ruhr,

Shiels,

Crossley

et al. 2024

Journal of Experimental Biology

View full text Add to dashboard Cite

Oxygen deprivation during embryonic development can permanently remodel the vertebrate heart, often causing cardiovascular abnormalities in adulthood. While this phenomenon is mostly damaging, recent evidence suggests developmental hypoxia produces stress-tolerant phenotypes in some ectothermic vertebrates. Embryonic common snapping turtles (Chelydra serpentina) subjected to chronic hypoxia display improved cardiac anoxia tolerance after hatching, which is associated with altered Ca2+ homeostasis in heart cells (cardiomyocytes). Here, we examined the possibility that changes in Ca2+ cycling, through the sarcoplasmic reticulum (SR), underlie the developmentally programmed cardiac phenotype of snapping turtles. We investigated this hypothesis by isolating cardiomyocytes from juvenile turtles that developed in either normoxia (21% O2; ‘N21’) or chronic hypoxia (10% O2; ‘H10’) and subjected the cells to anoxia/reoxygenation, in either the presence or absence of SR Ca2+-cycling inhibitors. We simultaneously measured cellular shortening, intracellular Ca2+ concentration ([Ca2+]i), and intracellular pH (pHi). Under normoxic conditions, N21 and H10 cardiomyocytes shortened equally, but H10 Ca2+ transients (Δ[Ca2+]i) were twofold smaller than those of N21 cells, and SR inhibition only decreased N21 shortening and Δ[Ca2+]i. Anoxia subsequently depressed shortening, Δ[Ca2+]i and pHi in control N21 and H10 cardiomyocytes, yet H10 shortening and Δ[Ca2+]i recovered to pre-anoxic levels, partly due to enhanced myofilament Ca2+ sensitivity. SR blockade abolished the recovery of anoxic H10 cardiomyocytes and potentiated decreases in shortening, Δ[Ca2+]i and pHi. Our novel results provide the first evidence of developmental programming of SR function and demonstrate that developmental hypoxia confers a long-lasting, superior anoxia-tolerant cardiac phenotype in snapping turtles, by modifying SR function and enhancing myofilament Ca2+ sensitivity.

show abstract

Epigenetic regulatory mechanism of macrophage polarization in diabetic wound healing (Review)

Song,

Wu,

Chen

et al. 2024

Mol Med Rep

View full text Add to dashboard Cite

Diabetic wounds represent a significant complication of diabetes and present a substantial challenge to global public health. Macrophages are crucial effector cells that play a pivotal role in the pathogenesis of diabetic wounds, through their polarization into distinct functional phenotypes. The field of epigenetics has emerged as a rapidly advancing research area, as this phenomenon has the potential to markedly affect gene expression, cellular differentiation, tissue development and susceptibility to disease. Understanding epigenetic mechanisms is crucial to further exploring disease pathogenesis. A growing body of scientific evidence has highlighted the pivotal role of epigenetics in the regulation of macrophage phenotypes. Various epigenetic mechanisms, such as DNA methylation, histone modification and non-coding RNAs, are involved in the modulation of macrophage phenotype differentiation in response to the various environmental stimuli present in diabetic wounds. The present review provided an overview of the various changes that take place in macrophage phenotypes and functions within diabetic wounds and discussed the emerging role of epigenetic modifications in terms of regulating macrophage plasticity in diabetic wounds. It is hoped that this synthesis of information will facilitate the elucidation of diabetic wound pathogenesis and the identification of potential therapeutic targets. Contents1. Introduction 2. Macrophage polarization 3. Macrophages in normal wound healing 4. Macrophages in diabetic wound healing 5. Epigenetic regulation of macrophage polarization in diabetic wounds 6. Interaction of epigenetic modifications regulating macrophage polarization in diabetic wounds 7. Key signaling pathways regulating macrophage polarization 8. Conclusion and perspectives

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Epigenetics in Heart Failure: Role of DNA Methylation in Potential Pathways Leading to Heart Failure with Preserved Ejection Fraction

Cited by 3 publications

References 101 publications

Exploring the therapeutic potential of tetrahydrobiopterin for heart failure with preserved ejection fraction: A path forward

Exploring the therapeutic potential of tetrahydrobiopterin for heart failure with preserved ejection fraction: A path forward

Developmental programming of sarcoplasmic reticulum function improves cardiac anoxia tolerance in turtles

Epigenetic regulatory mechanism of macrophage polarization in diabetic wound healing (Review)

Contact Info

Product

Resources

About