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Myocardial Infarction as a Consequence of Mitochondrial Dysfunction.
Wal, Pranay; Aziz, Namra; Singh, Yash Kumar; Wal, Ankita; Kosey, Sourabh; Rai, Awani Kumar.
Afiliação
  • Wal P; PSIT-Pranveer Singh Institute of Technology (Pharmacy), Bhauti, Kanpur, UP-209305, India.
  • Aziz N; PSIT-Pranveer Singh Institute of Technology (Pharmacy), Bhauti, Kanpur, UP-209305, India.
  • Singh YK; PSIT-Pranveer Singh Institute of Technology (Pharmacy), Bhauti, Kanpur, UP-209305, India.
  • Wal A; PSIT-Pranveer Singh Institute of Technology (Pharmacy), Bhauti, Kanpur, UP-209305, India.
  • Kosey S; Department of Pharmacy Practice, NIMS Institute of Pharmacy, NIMS University, Jaipur, Rajasthan, India.
  • Rai AK; PSIT-Pranveer Singh Institute of Technology (Pharmacy), Bhauti, Kanpur, UP-209305, India.
Curr Cardiol Rev ; 19(6): 23-30, 2023.
Article em En | MEDLINE | ID: mdl-37157208
ABSTRACT
Acute myocardial infarction is an event of myocardial necrosis caused by unstable ischemic syndrome. Myocardial infarction (MI) occurs when blood stops flowing to the cardiac tissue or myocardium and the heart muscle gets damaged due to poor perfusion and reduced oxygen supply. Mitochondria can serve as the arbiter of cell fate in response to stress. Oxidative metabolism is the function of mitochondria within the cell. Cardiac cells being highly oxidative tissue generates about 90% of their energy through oxidative metabolism. In this review, we focused on the role of mitochondria in energy generation in myocytes as well as its consequences on heart cells causing cell damage. The role of mitochondrial dysfunction due to oxidative stress, production of reactive oxygen species, and anaerobic production of lactate as a failure of oxidative metabolism are also discussed.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Miócitos Cardíacos / Infarto do Miocárdio Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Miócitos Cardíacos / Infarto do Miocárdio Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article