2. Academic Validation
  3. TRAP1 inhibits MIC60 ubiquitination to mitigate the injury of cardiomyocytes and protect mitochondria in extracellular acidosis

TRAP1 inhibits MIC60 ubiquitination to mitigate the injury of cardiomyocytes and protect mitochondria in extracellular acidosis

  • Cell Death Discov. 2021 Dec 14;7(1):389. doi: 10.1038/s41420-021-00786-5.
Lingxiao Zhang  # 1,  Ning Su  # 2,  Yuanyuan Luo 1,  Siyin Chen 1,  Tongfeng Zhao 3
Affiliations

Affiliations

  • 1 Departments of Endocrinology, the Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.
  • 2 Departments of Nephrology, the Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.
  • 3 Departments of Endocrinology, the Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China. zhaotf@mail.sysu.edu.cn.
  • # Contributed equally.
PMID: 34907169 DOI: 10.1038/s41420-021-00786-5
Abstract

Extracellular acidosis-induced mitochondrial damage of cardiomyocytes leads to cardiac dysfunction, but no detailed mechanism or efficient therapeutic target has been reported. Here we found that the protein levels of MIC60 were decreased in H9C2 cells and heart tissues in extracellular acidosis, which caused mitochondrial damage and cardiac dysfunction. Overexpression of MIC60 maintains H9C2 cells viability, increases ATP production and mitochondrial membrane potential, mitigates the disruptions of mitochondrial structure and cardiac injury. Mechanistically, extracellular acidosis excessively promoted MIC60 ubiquitin-dependent degradation. TRAP1 mitigated acidosis-induced mitochondrial impairments and cardiac injury by directly interacting with MIC60 to decrease its ubiquitin-dependent degradation in extracellular acidosis.

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