CHIP and aging: a key regulator of proteostasis and cellular senescence

被引：0

作者：

Surya Nath Pandey ^{[1
]}

Neetu Agrawal ^{[2
]}

Ehssan Moglad ^{[3
]}

G. Padma Priya ^{[4
]}

Manish Srivastava ^{[5
]}

Kattela Chennakesavulu ^{[6
]}

Biswaranjan Mohanty ^{[7
]}

Renu Arya ^{[8
]}

Imran Kazmi ^{[9
]}

Sami I. Alzarea ^{[10
]}

Waleed Hassan Almalk ^{[11
]}

Kavita Goyal ^{[12
]}

机构：

[1] Teerthanker Mahaveer University,Department of Pharmacology, Teerthanker Mahaveer College of Pharmacy

[2] Uttar Pradesh,Institute of Pharmaceutical Research

[3] GLA University,Department of Pharmaceutics, College of Pharmacy

[4] Uttar Pradesh,Department of Chemistry and Biochemistry, School of Sciences

[5] Prince Sattam Bin Abdulaziz University,Department of Endocrinology

[6] JAIN (Deemed to Be University),Department of Chemistry

[7] National Institute of Medical Sciences,Department of Nephrology IMS and SUM Hospital

[8] NIMS University,Department of Pharmacy

[9] Sathyabama Institute of Science and Technology,Department of Biochemistry, Faculty of Science

[10] Siksha ‘O’ Anusandhan (Deemed to Be University),Department of Pharmacology, College of Pharmacy

[11] Chandigarh Pharmacy College,University Medical Clinic

[12] Chandigarh Group of Colleges-Jhanjeri,undefined

[13] King Abdulaziz University,undefined

[14] Jouf University,undefined

[15] Umm Al-Qura University,undefined

[16] Department of Biotechnology,undefined

[17] Graphic Era (Deemed to Be University),undefined

来源：

Biogerontology | 2025年 / 26卷 / 3期

关键词：

CHIP; Ubiquitin–proteasome system; Cancer; Aging; Cellular Senescence; Neurodegeneration; Cardiovascular Aging; Autophagic Regulation;

D O I：

10.1007/s10522-025-10247-6

中图分类号：

学科分类号：

摘要：

Degradation of proteostasis, mitochondrial function, and cellular stress resistance results in a build-up of damaged proteins, oxidative insult, and chronic inflammation, characteristic of aging. CHIP is essential for maintaining protein quality control and cellular homeostasis by having dual E3 ubiquitin ligase and co-chaperone activities. CHIP facilitates proteostasis by maintaining proteostasis in misfolded, aggregated proteins by promoting their degradation. Mitochondrial dysfunction, oxidative imbalance, and cellular senescence are caused by its age-associated decline and contribute to neurodegenerative, cardiovascular, and oncogenic disease pathogenesis. Examples of recent pharmacological and gene-based strategies to correct CHIP and restore stress resilience have been made. This review examines the multiple facets of the aging role of CHIP and its potential as an aging disease therapy target.

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