Scholarlink

<p>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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

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

  • 期刊论文

  • 发表日期：

    2025年5月5日

查看全文
  • 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

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.