TY - JOUR
T1 - Mitochondrial Quality Control and Melatonin
T2 - A Strategy Against Myocardial Injury
AU - Ghavamikia, Nima
AU - Mehrnoosh, Faranak
AU - Zare, Farshad
AU - Ali-khiavi, Payam
AU - Sinehsepehr, Ali
AU - Boushehri, Yasaman Ghodsi
AU - Vahedinezhad, Milad
AU - Abdollahi, Elham
AU - Hjazi, Ahmed
AU - Aminnezhad, Siamak
AU - Saffarfar, Hossein
AU - Hamzehzadeh, Sina
AU - Nourizadeh, Mehrdad
AU - KarkonShayan, Sepideh
N1 - Publisher Copyright:
© 2025 Wiley Periodicals LLC.
PY - 2025/3
Y1 - 2025/3
N2 - Melatonin exhibits various biological functions, including regulation of circadian and endocrine rhythms, anti-inflammatory, and antioxidant effects. Aging and damaged mitochondria are major sources of oxidative stress (OS), and mitochondrial quality control (MQC) is crucial for maintaining normal mitochondrial function. Myocardial ischemia-reperfusion injury is a major complication that can arise during reperfusion therapy for coronary heart disease. However, effective intervention strategies are currently lacking. Mitochondrial dysfunction and OS are considered central mechanisms of myocardial reperfusion injury, with mitochondrial-targeted interventions being a potential treatment direction. Recent studies have shown that melatonin improves mitochondrial structure and function through multiple pathways. This review discusses the mechanisms by which melatonin ameliorates myocardial ischemia-reperfusion injury, focusing on MQC, and explores its potential applications in the prevention and treatment of myocardial ischemia-reperfusion injury.
AB - Melatonin exhibits various biological functions, including regulation of circadian and endocrine rhythms, anti-inflammatory, and antioxidant effects. Aging and damaged mitochondria are major sources of oxidative stress (OS), and mitochondrial quality control (MQC) is crucial for maintaining normal mitochondrial function. Myocardial ischemia-reperfusion injury is a major complication that can arise during reperfusion therapy for coronary heart disease. However, effective intervention strategies are currently lacking. Mitochondrial dysfunction and OS are considered central mechanisms of myocardial reperfusion injury, with mitochondrial-targeted interventions being a potential treatment direction. Recent studies have shown that melatonin improves mitochondrial structure and function through multiple pathways. This review discusses the mechanisms by which melatonin ameliorates myocardial ischemia-reperfusion injury, focusing on MQC, and explores its potential applications in the prevention and treatment of myocardial ischemia-reperfusion injury.
KW - melatonin
KW - melatonin receptors
KW - mitochondrial quality control
KW - myocardial ischemia-reperfusion injury
UR - http://www.scopus.com/inward/record.url?scp=85218966868&partnerID=8YFLogxK
U2 - 10.1002/jbt.70194
DO - 10.1002/jbt.70194
M3 - Review article
C2 - 40009050
AN - SCOPUS:85218966868
SN - 1095-6670
VL - 39
JO - Journal of Biochemical and Molecular Toxicology
JF - Journal of Biochemical and Molecular Toxicology
IS - 3
M1 - e70194
ER -
