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Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases

Physiological reactive oxygen species (ROS) are important regulators of intercellular signal transduction. Oxidative and antioxidation systems maintain a dynamic balance under physiological conditions. Increases in ROS levels destroy the dynamic balance, leading to oxidative stress damage. Oxidative...

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Autores principales: Cai, He, Liu, Yunxia, Men, Hongbo, Zheng, Yang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8222669/
https://www.ncbi.nlm.nih.gov/pubmed/34177809
http://dx.doi.org/10.3389/fendo.2021.683151
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author Cai, He
Liu, Yunxia
Men, Hongbo
Zheng, Yang
author_facet Cai, He
Liu, Yunxia
Men, Hongbo
Zheng, Yang
author_sort Cai, He
collection PubMed
description Physiological reactive oxygen species (ROS) are important regulators of intercellular signal transduction. Oxidative and antioxidation systems maintain a dynamic balance under physiological conditions. Increases in ROS levels destroy the dynamic balance, leading to oxidative stress damage. Oxidative stress is involved in the pathogenesis of aging-related cardiovascular diseases (ACVD), such as atherosclerosis, myocardial infarction, and heart failure, by contributing to apoptosis, hypertrophy, and fibrosis. Oxidative phosphorylation in mitochondria is the main source of ROS. Increasing evidence demonstrates the relationship between ACVD and humanin (HN), an endogenous peptide encoded by mitochondrial DNA. HN protects cardiomyocytes, endothelial cells, and fibroblasts from oxidative stress, highlighting its protective role in atherosclerosis, ischemia–reperfusion injury, and heart failure. Herein, we reviewed the signaling pathways associated with the HN effects on redox signals, including Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2), chaperone-mediated autophagy (CMA), c-jun NH2 terminal kinase (JNK)/p38 mitogen-activated protein kinase (p38 MAPK), adenosine monophosphate-activated protein kinase (AMPK), and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)-Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3). Furthermore, we discussed the relationship among HN, redox signaling pathways, and ACVD. Finally, we propose that HN may be a candidate drug for ACVD.
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spelling pubmed-82226692021-06-25 Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases Cai, He Liu, Yunxia Men, Hongbo Zheng, Yang Front Endocrinol (Lausanne) Endocrinology Physiological reactive oxygen species (ROS) are important regulators of intercellular signal transduction. Oxidative and antioxidation systems maintain a dynamic balance under physiological conditions. Increases in ROS levels destroy the dynamic balance, leading to oxidative stress damage. Oxidative stress is involved in the pathogenesis of aging-related cardiovascular diseases (ACVD), such as atherosclerosis, myocardial infarction, and heart failure, by contributing to apoptosis, hypertrophy, and fibrosis. Oxidative phosphorylation in mitochondria is the main source of ROS. Increasing evidence demonstrates the relationship between ACVD and humanin (HN), an endogenous peptide encoded by mitochondrial DNA. HN protects cardiomyocytes, endothelial cells, and fibroblasts from oxidative stress, highlighting its protective role in atherosclerosis, ischemia–reperfusion injury, and heart failure. Herein, we reviewed the signaling pathways associated with the HN effects on redox signals, including Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2), chaperone-mediated autophagy (CMA), c-jun NH2 terminal kinase (JNK)/p38 mitogen-activated protein kinase (p38 MAPK), adenosine monophosphate-activated protein kinase (AMPK), and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)-Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3). Furthermore, we discussed the relationship among HN, redox signaling pathways, and ACVD. Finally, we propose that HN may be a candidate drug for ACVD. Frontiers Media S.A. 2021-06-10 /pmc/articles/PMC8222669/ /pubmed/34177809 http://dx.doi.org/10.3389/fendo.2021.683151 Text en Copyright © 2021 Cai, Liu, Men and Zheng https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Cai, He
Liu, Yunxia
Men, Hongbo
Zheng, Yang
Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases
title Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases
title_full Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases
title_fullStr Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases
title_full_unstemmed Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases
title_short Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases
title_sort protective mechanism of humanin against oxidative stress in aging-related cardiovascular diseases
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8222669/
https://www.ncbi.nlm.nih.gov/pubmed/34177809
http://dx.doi.org/10.3389/fendo.2021.683151
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