TY - JOUR
T1 - CHIP and aging
T2 - a key regulator of proteostasis and cellular senescence
AU - Pandey, Surya Nath
AU - Agrawal, Neetu
AU - Moglad, Ehssan
AU - Priya, G. Padma
AU - Srivastava, Manish
AU - Chennakesavulu, Kattela
AU - Mohanty, Biswaranjan
AU - Arya, Renu
AU - Kazmi, Imran
AU - I. Alzarea, Sami
AU - Almalk, Waleed Hassan
AU - Goyal, Kavita
N1 - Publisher Copyright:
© The Author(s), under exclusive licence to Springer Nature B.V. 2025.
PY - 2025/6
Y1 - 2025/6
N2 - 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.
AB - 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.
KW - Aging
KW - Autophagic Regulation
KW - CHIP
KW - Cancer
KW - Cardiovascular Aging
KW - Cellular Senescence
KW - Neurodegeneration
KW - Ubiquitin–proteasome system
UR - http://www.scopus.com/inward/record.url?scp=105004260717&partnerID=8YFLogxK
U2 - 10.1007/s10522-025-10247-6
DO - 10.1007/s10522-025-10247-6
M3 - Review article
C2 - 40323531
AN - SCOPUS:105004260717
SN - 1389-5729
VL - 26
JO - Biogerontology
JF - Biogerontology
IS - 3
M1 - 104
ER -
