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

Surya Nath Pandey, Neetu Agrawal, Ehssan Moglad, G Padma Priya, Manish Srivastava, Kattela Chennakesavulu, Biswaranjan Mohanty, Renu Arya, Imran Kazmi, Sami I Alzarea, Waleed Hassan Almalk, Kavita Goyal

Department of Pharmacology, Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Uttar Pradesh, Moradabad, 244001, India.Department of Pharmacology, Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Uttar Pradesh, Moradabad, 244001, India. · pubmed

Paper

Abstract

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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Research summary

CHIP plays a crucial role in maintaining proteostasis and cellular homeostasis, which are essential for addressing the root causes of aging. The paper discusses how CHIP's decline contributes to aging-related diseases and explores potential therapeutic strategies, making it relevant to longevity research.

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