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Role of MST1 in the regulation of autophagy and mitophagy: implications for aging-related diseases

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Abstract

As a key mechanism to maintain cellular homeostasis under stress conditions, autophagy/mitophagy is related to the occurrence of metabolic disorders, neurodegenerative diseases, cancer, and other aging-related diseases, but the relevant signal pathways regulating autophagy have not been clarified. Mammalian sterile 20-like kinase 1 (MST1) is a central regulatory protein of many metabolic pathways involved in the pathophysiological processes of aging and aging-related diseases and has become a critical integrator affecting autophagic signaling. Recent studies show that MST1 not only suppresses autophagy through directly phosphorylating Beclin-1 and/or inhibiting the protein expression of silent information regulator 1 (SIRT1) in the cytoplasm, but also inhibits BCL2/adenovirus E1B protein-interacting protein 3 (BNIP3)–, FUN14 domain containing 1 (FUNDC1)–, and Parkin (Parkinson protein 2)–mediated mitophagy by interacting with factors such as Ras association domain family 1A (RASSF1A). Indeed, a common pharmacological strategy for anti-aging is to induce autophagy/mitophagy through MST1 inhibition. This article reviews the role and mechanism of MST1 in regulating autophagy during aging, to provide evidence for the development of drugs targeting MST1.

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Funding

This work was supported by grants from the National Natural Science Foundation of China (31900842, 31960192), the Innovative Project of Institute of Sports Medicine and Health of Chengdu Sport University (CX21A01), the Jiangxi Provincial Science Fund for Distinguished Young Scholars (No. 20202ACBL216004), and the Jiangxi Provincial Natural Science Foundation (No. 20192BAB205081).

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Author notes

  1. Huayu Shang, Trisha A. VanDusseldorp, Ranggui Ma, and Yan Zhao have contributed equally to this work.

Authors and Affiliations

  1. School of Sports Medicine and Health, Chengdu Sport University, Chengdu, China

    Huayu Shang & Ranggui Ma

  2. Department of Exercise Science and Sport Management, Kennesaw State University, Kennesaw, GA, USA

    Trisha A. VanDusseldorp

  3. Exercise Physiology and Biochemistry Laboratory, College of Physical Education and Health, Wenzhou University, Wenzhou, China

    Yan Zhao & Zhi Xia

  4. Department of Exercise Physiology, University of Lynchburg, Lynchburg, VA, USA

    Jason Cholewa

  5. Department of Physical Education, Federal University of Maranhão (UFMA), Sao Luis, MA, Brazil

    Nelo Eidy Zanchi

  6. Laboratory of Skeletal Muscle Biology and Human Strength Performance (LABFORCEH), Sao Luis, MA, Brazil

    Nelo Eidy Zanchi

  7. Exercise Physiology and Biochemistry Laboratory, College of Physical Education, Jinggangshan University, Ji’an, China

    Zhi Xia

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  1. Huayu Shang
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Contributions

Huayu Shang and Zhi Xia designed the research and made the literature selection. Huayu Shang, Trisha VanDusseldorp, Ranggui Ma, and Yan Zhao wrote the paper. Jason Cholewa, Nelo Eidy Zanchi, and Zhi Xia revised the paper. All the authors declare that all data were generated in-house and that no paper mill was used.

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Correspondence to Zhi Xia.

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Key points

1. MST1 suppresses autophagy or mitophagy through multiple signalings.

2. Inhibiting MST1 to induce autophagy or mitophagy modulates aging-related diseases.

3. Interventional strategies targeting MST1 could promote healthy aging.

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Shang, H., VanDusseldorp, T.A., Ma, R. et al. Role of MST1 in the regulation of autophagy and mitophagy: implications for aging-related diseases. J Physiol Biochem 78, 709–719 (2022). https://doi.org/10.1007/s13105-022-00904-6

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