FGF1ΔHBS prevents diabetic cardiomyopathy by maintaining mitochondrial homeostasis and reducing oxidative stress via AMPK/Nur77 suppression DOI Creative Commons
Dezhong Wang, Yuan Yin, Shu‐Yi Wang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2021, Volume and Issue: 6(1)

Published: March 24, 2021

Abstract As a classically known mitogen, fibroblast growth factor 1 (FGF1) has been found to exert other pleiotropic functions such as metabolic regulation and myocardial protection. Here, we show that serum levels of FGF1 were decreased positively correlated with fraction shortening in diabetic cardiomyopathy (DCM) patients, indicating is potential therapeutic target for DCM. We treatment variant (FGF1 ∆HBS ) reduced proliferative potency prevented diabetes-induced cardiac injury remodeling restored function. RNA-Seq results obtained from the tissues db/db mice showed significant increase expression anti-oxidative genes decrease Nur77 by treatment. Both vivo vitro studies indicate exerted these beneficial effects markedly reducing mitochondrial fragmentation, reactive oxygen species (ROS) generation cytochrome c leakage enhancing respiration rate β-oxidation 5’ AMP-activated protein kinase (AMPK)/Nur77-dependent manner, all which not observed AMPK null mice. The favorable activity properties testify its promising use DCM disorders.

Language: Английский

Mitochondrial Function and Dysfunction in Dilated Cardiomyopathy DOI Creative Commons
Daniela Ramaccini,

Vanessa Montoya‐Uribe,

Femke J. Aan

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2021, Volume and Issue: 8

Published: Jan. 12, 2021

Cardiac tissue requires a persistent production of energy in order to exert its pumping function. Therefore, the maintenance this function relies on mitochondria that represent “powerhouse” all cardiac activities. Mitochondria being one key players for proper functioning mammalian heart suggests continual regulation and organization. adapt cellular demands via fusion-fission events and, as proof-reading ability, undergo mitophagy cases abnormalities. Ca 2+ fluxes play pivotal role regulating mitochondrial functions, including ATP production, metabolism, oxidative stress balance apoptosis. Communication between others organelles, especially sarcoplasmic reticulum is required optimal Consequently, abnormal activity results decreased leading pathological conditions. In review, we will describe how or dysfunction impacts activities development dilated cardiomyopathy.

Language: Английский

Citations

97

Mitochondria-Associated Endoplasmic Reticulum Membranes in Cardiovascular Diseases DOI Creative Commons
Peng Gao, Zhencheng Yan, Zhiming Zhu

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2020, Volume and Issue: 8

Published: Nov. 9, 2020

The endoplasmic reticulum (ER) and mitochondria are physically connected to form dedicated structural domains known as mitochondria-associated ER membranes (MAMs), which participate in fundamental biological processes, including lipid calcium (Ca2+) homeostasis, mitochondrial dynamics other related cellular behaviors such autophagy, stress, inflammation apoptosis. Many studies have proved the importance of MAMs maintaining normal function both organelles, abnormal amount, structure or is occurrence cardiovascular diseases. Here, we review knowledge regarding components according their different functions specific roles physiology pathophysiology, focusing on some highly prevalent diseases, ischemia-reperfusion, diabetic cardiomyopathy, heart failure, pulmonary arterial hypertension systemic vascular Finally, summarize possible mechanisms MAM diseases put forward obstacles understanding may encounter.

Language: Английский

Citations

94

HSF1 functions as a key defender against palmitic acid-induced ferroptosis in cardiomyocytes DOI
Nian Wang, Heng Ma, Jing Li

et al.

Journal of Molecular and Cellular Cardiology, Journal Year: 2020, Volume and Issue: 150, P. 65 - 76

Published: Oct. 22, 2020

Language: Английский

Citations

93

Physical Exercise: A Novel Tool to Protect Mitochondrial Health DOI Creative Commons
Daniela Sorriento,

Eugenio Di Vaia,

Guido Iaccarino

et al.

Frontiers in Physiology, Journal Year: 2021, Volume and Issue: 12

Published: April 27, 2021

Mitochondrial dysfunction is a crucial contributor to heart diseases. Alterations in energetic metabolism affect homeostatic processes, such asATP production, the generation of reactive oxygen species, and release pro-apoptotic factors, associated with metabolic abnormalities. In response deficiency, cardiomyocytes activate Quality Control (MQC), critical process maintaining mitochondrial health. This compromised cardiovascular diseases depending on pathology's severity represents, therefore, potential therapeutic target. Several targeting molecules within this have been identified last years, strategies proposed ameliorate mitochondria monitoring function. context, physical exercise considered non-pharmacological strategy protect Physical regulates MQC allowing repair/elimination damaged synthesizing new ones, thus recovering state. review, we will deal effect cardiac function tracing its ability modulate specific steps both physiologic pathologic conditions.

Language: Английский

Citations

78

FGF1ΔHBS prevents diabetic cardiomyopathy by maintaining mitochondrial homeostasis and reducing oxidative stress via AMPK/Nur77 suppression DOI Creative Commons
Dezhong Wang, Yuan Yin, Shu‐Yi Wang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2021, Volume and Issue: 6(1)

Published: March 24, 2021

Abstract As a classically known mitogen, fibroblast growth factor 1 (FGF1) has been found to exert other pleiotropic functions such as metabolic regulation and myocardial protection. Here, we show that serum levels of FGF1 were decreased positively correlated with fraction shortening in diabetic cardiomyopathy (DCM) patients, indicating is potential therapeutic target for DCM. We treatment variant (FGF1 ∆HBS ) reduced proliferative potency prevented diabetes-induced cardiac injury remodeling restored function. RNA-Seq results obtained from the tissues db/db mice showed significant increase expression anti-oxidative genes decrease Nur77 by treatment. Both vivo vitro studies indicate exerted these beneficial effects markedly reducing mitochondrial fragmentation, reactive oxygen species (ROS) generation cytochrome c leakage enhancing respiration rate β-oxidation 5’ AMP-activated protein kinase (AMPK)/Nur77-dependent manner, all which not observed AMPK null mice. The favorable activity properties testify its promising use DCM disorders.

Language: Английский

Citations

76