Basic & Clinical Medicine ›› 2025, Vol. 45 ›› Issue (1): 126-129.doi: 10.16352/j.issn.1001-6325.2025.01.0126

• Mini Reviews • Previous Articles     Next Articles

Role of mitochondrial fusion in doxorubicin-induced cardiotoxicity

WANG Yuqi1, WANG Xinyu1, LUO Haowen1, LU Zhaoxin1, ZHAO Yiwei1, CHANG Pan2*   

  1. 1. Department of Anesthesia,Second Clinical Medical College, Xi′an Medical College, Xi′an 710038;
    2. Department of Physiology and Pathophysiology, Basic Department, Air Force Medical University, Xi′an 710000, China
  • Received:2024-05-16 Revised:2024-07-15 Online:2025-01-05 Published:2024-12-25
  • Contact: *herepanpan@163.com

Abstract: Adriamycin is a widely used anti-tumor drug. Targeting mitochondrial fusion proteins/mitofusion 1/2(MFN1/2) and nuclear factor-erythroid 2-related factor 2(NRF2) can up-regulate the expression of mitochondrial fusion protein through PKCε/Stat3/MFN2, SIRT1/MFN2, AMPK/NRF2 and other signaling pathways, promote mitochondrial fusion, maintain kinetic balance and protect mitochondrial function, reduce myocardial cell apoptosis and reduce cardiac toxicity. Understanding the regulatory role and mechanism of mitochondrial fusion in doxorubicin-induced cardio toxicity will provide new strategies for the prevention and treatment of diseases.

Key words: doxorubicin, mitochondrial fusion, cardiotoxicity, mitofusin(MFN1/2), nuclear factor-erythroid 2-related factor 2(NRF2)

CLC Number: