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Review Article | Open Access

The functional role of Higd1a in mitochondrial homeostasis and in multiple disease processes

Jie-Ying Zhua,bMin Chena,bWang-Jing Mua,bHong-Yang Luoa,bLiang Guoa,b,( )
School of Kinesiology, Shanghai University of Sport, Shanghai 200438, China
Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, Shanghai University of Sport, Shanghai 200438, China

Peer review under responsibility of Chongqing Medical University.

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Abstract

Higd1a is a conserved gene in evolution which is widely expressed in many tissues in mammals. Accumulating evidence has revealed multiple functions of Higd1a, as a mitochondrial inner membrane protein, in the regulation of metabolic homeostasis. It plays an important role in anti-apoptosis and promotes cellular survival in several cell types under hypoxic condition. And the survival of porcine Sertoli cells facilitated by Higd1a helps to support reproduction. In some cases, Higd1a can serve as a sign of metabolic stress. Over the past several years, a considerable amount of studies about how tumor fate is determined and how cancerous proliferation is regulated by Higd1a have been performed. In this review, we summarize the physiological functions of Higd1a in metabolic homeostasis and its pathophysiological roles in distinct diseases including cancer, nonalcoholic fatty liver disease (NAFLD), type Ⅱ diabetes and mitochondrial diseases. The prospect of Higd1a with potential to preserve mammal health is also discussed. This review might pave the way for Higd1a-based research and application in clinical practice.

Genes & Diseases
Pages 1833-1845
Cite this article:
Zhu J-Y, Chen M, Mu W-J, et al. The functional role of Higd1a in mitochondrial homeostasis and in multiple disease processes. Genes & Diseases, 2023, 10(5): 1833-1845. https://doi.org/10.1016/j.gendis.2022.03.018

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Received: 24 December 2021
Revised: 04 March 2022
Accepted: 22 March 2022
Published: 22 April 2022
© 2022 The Authors.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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