Role of mitochondrial quality surveillance in myocardial infarction: From bench to bedside

•Mitochondrial quality surveillance is regulated by a variety of adaptive responses.•Mitochondrial fission favors the elimination of depolarized mitochondria through mitophagy.•The double-edge sword of mitophagy needs to be taken into consideration in the conception of new pharmacological approaches...

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Bibliographic Details
Published inAgeing research reviews Vol. 66; p. 101250
Main Authors Zhou, Hao, Ren, Jun, Toan, Sam, Mui, David
Format Journal Article
LanguageEnglish
Published England Elsevier B.V 01.03.2021
Subjects
Fission
Fusion
Humans
Mitochondria
Mitochondrial Dynamics
Mitochondrial Proteins
Mitochondrial quality surveillance
Mitophagy
Myocardial Infarction
Proteostasis
Myocardial infarction
Mitochondrial quality surveillance
Proteostasis
Mitophagy
Fusion
Fission
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Abstract •Mitochondrial quality surveillance is regulated by a variety of adaptive responses.•Mitochondrial fission favors the elimination of depolarized mitochondria through mitophagy.•The double-edge sword of mitophagy needs to be taken into consideration in the conception of new pharmacological approaches to treat MI.•Mitochondrial biogenesis represents a regenerative program to replace old and damaged mitochondria with new and healthy ones.•Mitochondrial bioenergetics is regulated by a metabolic switch between glucose and fatty acid usage, depending on oxygen availability. Myocardial infarction (MI) is the irreversible death of cardiomyocyte secondary to prolonged lack of oxygen or fresh blood supply. Historically considered as merely cardiomyocyte powerhouse that manufactures ATP and other metabolites, mitochondrion is recently being identified as a signal regulator that is implicated in the crosstalk and signal integration of cardiomyocyte contraction, metabolism, inflammation, and death. Mitochondria quality surveillance is an integrated network system modifying mitochondrial structure and function through the coordination of various processes including mitochondrial fission, fusion, biogenesis, bioenergetics, proteostasis, and degradation via mitophagy. Mitochondrial fission favors the elimination of depolarized mitochondria through mitophagy, whereas mitochondrial fusion preserves the mitochondrial network upon stress through integration of two or more small mitochondria into an interconnected phenotype. Mitochondrial biogenesis represents a regenerative program to replace old and damaged mitochondria with new and healthy ones. Mitochondrial bioenergetics is regulated by a metabolic switch between glucose and fatty acid usage, depending on oxygen availability. To maintain the diversity and function of mitochondrial proteins, a specialized protein quality control machinery regulates protein dynamics and function through the activity of chaperones and proteases, and induction of the mitochondrial unfolded protein response. In this review, we provide an overview of the molecular mechanisms governing mitochondrial quality surveillance and highlight the most recent preclinical and clinical therapeutic approaches to restore mitochondrial fitness during both MI and post-MI heart failure.
AbstractList •Mitochondrial quality surveillance is regulated by a variety of adaptive responses.•Mitochondrial fission favors the elimination of depolarized mitochondria through mitophagy.•The double-edge sword of mitophagy needs to be taken into consideration in the conception of new pharmacological approaches to treat MI.•Mitochondrial biogenesis represents a regenerative program to replace old and damaged mitochondria with new and healthy ones.•Mitochondrial bioenergetics is regulated by a metabolic switch between glucose and fatty acid usage, depending on oxygen availability. Myocardial infarction (MI) is the irreversible death of cardiomyocyte secondary to prolonged lack of oxygen or fresh blood supply. Historically considered as merely cardiomyocyte powerhouse that manufactures ATP and other metabolites, mitochondrion is recently being identified as a signal regulator that is implicated in the crosstalk and signal integration of cardiomyocyte contraction, metabolism, inflammation, and death. Mitochondria quality surveillance is an integrated network system modifying mitochondrial structure and function through the coordination of various processes including mitochondrial fission, fusion, biogenesis, bioenergetics, proteostasis, and degradation via mitophagy. Mitochondrial fission favors the elimination of depolarized mitochondria through mitophagy, whereas mitochondrial fusion preserves the mitochondrial network upon stress through integration of two or more small mitochondria into an interconnected phenotype. Mitochondrial biogenesis represents a regenerative program to replace old and damaged mitochondria with new and healthy ones. Mitochondrial bioenergetics is regulated by a metabolic switch between glucose and fatty acid usage, depending on oxygen availability. To maintain the diversity and function of mitochondrial proteins, a specialized protein quality control machinery regulates protein dynamics and function through the activity of chaperones and proteases, and induction of the mitochondrial unfolded protein response. In this review, we provide an overview of the molecular mechanisms governing mitochondrial quality surveillance and highlight the most recent preclinical and clinical therapeutic approaches to restore mitochondrial fitness during both MI and post-MI heart failure.
Myocardial infarction (MI) is the irreversible death of cardiomyocyte secondary to prolonged lack of oxygen or fresh blood supply. Historically considered as merely cardiomyocyte powerhouse that manufactures ATP and other metabolites, mitochondrion is recently being identified as a signal regulator that is implicated in the crosstalk and signal integration of cardiomyocyte contraction, metabolism, inflammation, and death. Mitochondria quality surveillance is an integrated network system modifying mitochondrial structure and function through the coordination of various processes including mitochondrial fission, fusion, biogenesis, bioenergetics, proteostasis, and degradation via mitophagy. Mitochondrial fission favors the elimination of depolarized mitochondria through mitophagy, whereas mitochondrial fusion preserves the mitochondrial network upon stress through integration of two or more small mitochondria into an interconnected phenotype. Mitochondrial biogenesis represents a regenerative program to replace old and damaged mitochondria with new and healthy ones. Mitochondrial bioenergetics is regulated by a metabolic switch between glucose and fatty acid usage, depending on oxygen availability. To maintain the diversity and function of mitochondrial proteins, a specialized protein quality control machinery regulates protein dynamics and function through the activity of chaperones and proteases, and induction of the mitochondrial unfolded protein response. In this review, we provide an overview of the molecular mechanisms governing mitochondrial quality surveillance and highlight the most recent preclinical and clinical therapeutic approaches to restore mitochondrial fitness during both MI and post-MI heart failure.Myocardial infarction (MI) is the irreversible death of cardiomyocyte secondary to prolonged lack of oxygen or fresh blood supply. Historically considered as merely cardiomyocyte powerhouse that manufactures ATP and other metabolites, mitochondrion is recently being identified as a signal regulator that is implicated in the crosstalk and signal integration of cardiomyocyte contraction, metabolism, inflammation, and death. Mitochondria quality surveillance is an integrated network system modifying mitochondrial structure and function through the coordination of various processes including mitochondrial fission, fusion, biogenesis, bioenergetics, proteostasis, and degradation via mitophagy. Mitochondrial fission favors the elimination of depolarized mitochondria through mitophagy, whereas mitochondrial fusion preserves the mitochondrial network upon stress through integration of two or more small mitochondria into an interconnected phenotype. Mitochondrial biogenesis represents a regenerative program to replace old and damaged mitochondria with new and healthy ones. Mitochondrial bioenergetics is regulated by a metabolic switch between glucose and fatty acid usage, depending on oxygen availability. To maintain the diversity and function of mitochondrial proteins, a specialized protein quality control machinery regulates protein dynamics and function through the activity of chaperones and proteases, and induction of the mitochondrial unfolded protein response. In this review, we provide an overview of the molecular mechanisms governing mitochondrial quality surveillance and highlight the most recent preclinical and clinical therapeutic approaches to restore mitochondrial fitness during both MI and post-MI heart failure.
Myocardial infarction (MI) is the irreversible death of cardiomyocyte secondary to prolonged lack of oxygen or fresh blood supply. Historically considered as merely cardiomyocyte powerhouse that manufactures ATP and other metabolites, mitochondrion is recently being identified as a signal regulator that is implicated in the crosstalk and signal integration of cardiomyocyte contraction, metabolism, inflammation, and death. Mitochondria quality surveillance is an integrated network system modifying mitochondrial structure and function through the coordination of various processes including mitochondrial fission, fusion, biogenesis, bioenergetics, proteostasis, and degradation via mitophagy. Mitochondrial fission favors the elimination of depolarized mitochondria through mitophagy, whereas mitochondrial fusion preserves the mitochondrial network upon stress through integration of two or more small mitochondria into an interconnected phenotype. Mitochondrial biogenesis represents a regenerative program to replace old and damaged mitochondria with new and healthy ones. Mitochondrial bioenergetics is regulated by a metabolic switch between glucose and fatty acid usage, depending on oxygen availability. To maintain the diversity and function of mitochondrial proteins, a specialized protein quality control machinery regulates protein dynamics and function through the activity of chaperones and proteases, and induction of the mitochondrial unfolded protein response. In this review, we provide an overview of the molecular mechanisms governing mitochondrial quality surveillance and highlight the most recent preclinical and clinical therapeutic approaches to restore mitochondrial fitness during both MI and post-MI heart failure.
ArticleNumber 101250
Author Zhou, Hao
Ren, Jun
Mui, David
Toan, Sam
Author_xml – sequence: 1
  givenname: Hao
  orcidid: 0000-0001-8138-7275
  surname: Zhou
  fullname: Zhou, Hao
  email: zhouhao@plagh.org, zhouhao301@outlook.com
  organization: Department of Cardiology, Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing 100853, China
– sequence: 2
  givenname: Jun
  surname: Ren
  fullname: Ren, Jun
  organization: Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA
– sequence: 3
  givenname: Sam
  surname: Toan
  fullname: Toan, Sam
  organization: Department of Chemical Engineering, University of Minnesota-Duluth, Duluth, MN 55812, USA
– sequence: 4
  givenname: David
  surname: Mui
  fullname: Mui, David
  organization: Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33388396$$D View this record in MEDLINE/PubMed
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Mitophagy
Fusion
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Snippet •Mitochondrial quality surveillance is regulated by a variety of adaptive responses.•Mitochondrial fission favors the elimination of depolarized mitochondria...
Myocardial infarction (MI) is the irreversible death of cardiomyocyte secondary to prolonged lack of oxygen or fresh blood supply. Historically considered as...
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SubjectTerms Fission
Fusion
Humans
Mitochondria
Mitochondrial Dynamics
Mitochondrial Proteins
Mitochondrial quality surveillance
Mitophagy
Myocardial Infarction
Proteostasis
Title Role of mitochondrial quality surveillance in myocardial infarction: From bench to bedside
URI https://www.clinicalkey.com/#!/content/1-s2.0-S1568163720303858
https://dx.doi.org/10.1016/j.arr.2020.101250
https://www.ncbi.nlm.nih.gov/pubmed/33388396
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