Scholarlink

<p>Mitochondria–endoplasmic reticulum (ER) contact sites (MERCS) are nanoscopic, dynamic platforms integrating metabolism, signaling, and stress responses to regulate cell fate. These nanoscopic interfaces remodel continuously to meet the demands of proliferating, quiescent, and senescent cells. We synthesize evidence that MERCS actively coordinate local Ca<sup>2+</sup> signaling, non-vesicular lipid transfer, and proteostasis to shape mitochondrial function and cellular homeostasis. We discuss how MERCS architecture changes across the cell cycle and during arrest, distinguishing adaptive from maladaptive remodeling, and consider therapeutic potential in aging and age-related disease.</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

Mitochondria–ER contact sites (MERCS) in the cell cycle: molecular architecture and functional remodeling across cellular states

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月27日

查看全文
  • Eduardo Silva-Pavez,
  • Bruno Torres-Gonzalez,
  • Michelle Sotomayor,
  • Benjamín Cartes-Saavedra,
  • Dorian V. Ziegler,
  • Yessia Hidalgo-Fadic,
  • Ulises Ahumada-Castro

摘要

Mitochondria–endoplasmic reticulum (ER) contact sites (MERCS) are nanoscopic, dynamic platforms integrating metabolism, signaling, and stress responses to regulate cell fate. These nanoscopic interfaces remodel continuously to meet the demands of proliferating, quiescent, and senescent cells. We synthesize evidence that MERCS actively coordinate local Ca2+ signaling, non-vesicular lipid transfer, and proteostasis to shape mitochondrial function and cellular homeostasis. We discuss how MERCS architecture changes across the cell cycle and during arrest, distinguishing adaptive from maladaptive remodeling, and consider therapeutic potential in aging and age-related disease.