Mitochondrial dysfunction in lipid processing and gastrointestinal disorders

Yan Hu; Hao Huang; Rong Xiang

doi:10.1016/j.tem.2024.02.009

Mitochondrial dysfunction in lipid processing and gastrointestinal disorders

Trends Endocrinol Metab. 2024 Feb 27:S1043-2760(24)00038-9. doi: 10.1016/j.tem.2024.02.009. Online ahead of print.

Authors

Yan Hu¹, Hao Huang², Rong Xiang³

Affiliations

¹ Key Laboratory of Birth Defects and Related Diseases of Women and Children, Ministry of Education (MOE), State Key Laboratory of Biotherapy, West China Second University Hospital, Sichuan University, Chengdu, China.
² Department of Cell Biology, School of Life Sciences, Central South University, Changsha, China; Hunan Key Laboratory of Organ Fibrosis, Central South University, Changsha, China. Electronic address: xyskhuanghao@csu.edu.cn.
³ Department of Cell Biology, School of Life Sciences, Central South University, Changsha, China; Hunan Key Laboratory of Organ Fibrosis, Central South University, Changsha, China. Electronic address: shirlesmile@csu.edu.cn.

PMID: 38418280
DOI: 10.1016/j.tem.2024.02.009

Abstract

Mitochondrial dysfunctions predominantly cause encephalomyopathies with muscle atrophy and neurodegeneration. However, their impact on other tissues, particularly the gastrointestinal tract, requires further investigation. In a recent report in Nature, Moschandrea et al. used mice deficient in the mitochondrial aminoacyl-tRNA synthetase DARS2 to investigate the role of enterocytic mitochondria in dietary lipid processing and transport. Their work sheds light on the development of gastrointestinal disorders as a result of mitochondrial dysfunction.

Keywords: DARS2; gastrointestinal disorders; lipid processing; mitochondria; mitochondrial aminoacyl-tRNA synthetases (mt-AaRSs).