Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases

Yunhao Li,1,* Ningning Zheng,2,* Xudong Ding3 1The First Clinical College, China Medical University, Shenyang, Liaoning, People’s Republic of China; 2Department of Pathophysiology, College of Basic Medical Science, China Medical University, Shenyang, Liaoning, People’s Republic of Ch...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Li Y, Zheng N, Ding X
Formato: article
Lenguaje:EN
Publicado: Dove Medical Press 2021
Materias:
Acceso en línea:https://doaj.org/article/b8565df62fa741cc8ff7dd02cecce22c
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:b8565df62fa741cc8ff7dd02cecce22c
record_format dspace
spelling oai:doaj.org-article:b8565df62fa741cc8ff7dd02cecce22c2021-11-25T18:55:29ZMitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases1178-7007https://doaj.org/article/b8565df62fa741cc8ff7dd02cecce22c2021-11-01T00:00:00Zhttps://www.dovepress.com/mitophagy-disequilibrium-a-prominent-pathological-mechanism-in-metabol-peer-reviewed-fulltext-article-DMSOhttps://doaj.org/toc/1178-7007Yunhao Li,1,* Ningning Zheng,2,* Xudong Ding3 1The First Clinical College, China Medical University, Shenyang, Liaoning, People’s Republic of China; 2Department of Pathophysiology, College of Basic Medical Science, China Medical University, Shenyang, Liaoning, People’s Republic of China; 3Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xudong DingDepartment of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, 110004, People’s Republic of ChinaTel +8618940257698Email dingxd@sj-hospital.orgAbstract: With overall food intake among the general population as high as ever, metabolic syndrome (MetS) has become a global epidemic and is responsible for many serious life-threatening diseases, especially heart failure. In multiple metabolic disorders, maintaining a dynamic balance of mitochondrial number and function is necessary to prevent the overproduction of reactive oxygen species (ROS), which has been proved to be one of the important mechanisms of cardiomyocyte injury due to the mismatching of oxygen consumption and mitochondrial population and finally to heart failure. Mitophagy is a process that eliminates damaged or redundant mitochondria. It is mediated by a series of signaling molecules, including PINK, parkin, BINP3, FUNDC1, CTSD, Drp1, Rab9 and mTOR. Meanwhile, increasing evidence also showed that the interaction between ferroptosis and mitophagy interfered with mitochondrial homeostasis. This review will focus on these essential molecules and pathways of mitophagy and cell homeostasis affected by hypoxia and other stimuli in metabolic heart diseases.Keywords: mitophagy, metabolic heart diseases, metabolic syndrome, PTEN induced putative kinase, PINK, parkin, Bcl-2/E1B19kDa-interacting protein, BNIP3, FUN14 domain-containing protein 1, FUNDC1, ferroptosisLi YZheng NDing XDove Medical Pressarticlemitophagymetabolic heart diseasesmetabolic syndromepten induced putative kinase (pink)parkinbcl-2/e1b19kda-interacting protein(bnip3)fun14 domain-containing protein 1(fundc1)ferroptosisSpecialties of internal medicineRC581-951ENDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy, Vol Volume 14, Pp 4631-4640 (2021)
institution DOAJ
collection DOAJ
language EN
topic mitophagy
metabolic heart diseases
metabolic syndrome
pten induced putative kinase (pink)
parkin
bcl-2/e1b19kda-interacting protein(bnip3)
fun14 domain-containing protein 1(fundc1)
ferroptosis
Specialties of internal medicine
RC581-951
spellingShingle mitophagy
metabolic heart diseases
metabolic syndrome
pten induced putative kinase (pink)
parkin
bcl-2/e1b19kda-interacting protein(bnip3)
fun14 domain-containing protein 1(fundc1)
ferroptosis
Specialties of internal medicine
RC581-951
Li Y
Zheng N
Ding X
Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases
description Yunhao Li,1,* Ningning Zheng,2,* Xudong Ding3 1The First Clinical College, China Medical University, Shenyang, Liaoning, People’s Republic of China; 2Department of Pathophysiology, College of Basic Medical Science, China Medical University, Shenyang, Liaoning, People’s Republic of China; 3Department of Anesthesiology, Shengjing Hospital of China Medical University, Shenyang, Liaoning, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xudong DingDepartment of Anesthesiology, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Shenyang, 110004, People’s Republic of ChinaTel +8618940257698Email dingxd@sj-hospital.orgAbstract: With overall food intake among the general population as high as ever, metabolic syndrome (MetS) has become a global epidemic and is responsible for many serious life-threatening diseases, especially heart failure. In multiple metabolic disorders, maintaining a dynamic balance of mitochondrial number and function is necessary to prevent the overproduction of reactive oxygen species (ROS), which has been proved to be one of the important mechanisms of cardiomyocyte injury due to the mismatching of oxygen consumption and mitochondrial population and finally to heart failure. Mitophagy is a process that eliminates damaged or redundant mitochondria. It is mediated by a series of signaling molecules, including PINK, parkin, BINP3, FUNDC1, CTSD, Drp1, Rab9 and mTOR. Meanwhile, increasing evidence also showed that the interaction between ferroptosis and mitophagy interfered with mitochondrial homeostasis. This review will focus on these essential molecules and pathways of mitophagy and cell homeostasis affected by hypoxia and other stimuli in metabolic heart diseases.Keywords: mitophagy, metabolic heart diseases, metabolic syndrome, PTEN induced putative kinase, PINK, parkin, Bcl-2/E1B19kDa-interacting protein, BNIP3, FUN14 domain-containing protein 1, FUNDC1, ferroptosis
format article
author Li Y
Zheng N
Ding X
author_facet Li Y
Zheng N
Ding X
author_sort Li Y
title Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases
title_short Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases
title_full Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases
title_fullStr Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases
title_full_unstemmed Mitophagy Disequilibrium, a Prominent Pathological Mechanism in Metabolic Heart Diseases
title_sort mitophagy disequilibrium, a prominent pathological mechanism in metabolic heart diseases
publisher Dove Medical Press
publishDate 2021
url https://doaj.org/article/b8565df62fa741cc8ff7dd02cecce22c
work_keys_str_mv AT liy mitophagydisequilibriumaprominentpathologicalmechanisminmetabolicheartdiseases
AT zhengn mitophagydisequilibriumaprominentpathologicalmechanisminmetabolicheartdiseases
AT dingx mitophagydisequilibriumaprominentpathologicalmechanisminmetabolicheartdiseases
_version_ 1718410548827127808