Scholarlink

<p>Tendon stem/progenitor cell (TSPC) senescence contributes to age-related tendon degeneration, yet the molecular mechanisms underlying this process remain poorly understood. In present study, we investigated the role of High-Mobility Group A2 (HMGA2) in TSPCs senescence. During the tendon aging, we showed that HMGA2 expression decreases with age. In senescent TSPCs, HMGA2 overexpression significantly delayed TSPCs senescence. Additionally, overexpression of HMGA2 restored the age-related dysfunction of migration, tenogenic differentiation, and mitophagy. HMGA2 also suppressed the senescence-associated secretory phenotype (SASP), downregulating inflammatory cytokines such as IL-1β, IL-6, and TGF-β. Furthermore, we suggested that the PI3K-AKT signaling pathway is activated in senescent TSPCs, and HMGA2 overexpression could inhibit the PI3K-AKT signaling pathway activation, which demonstrates that HMGA2 might attenuate senescence and age-related dysfunction of TSPCs through the repression of PI3K-AKT signaling pathway. Our findings collectively indicated the crucial involvement of HMGA2 in TSPCs senescence regulation and suggested a novel target for preventing tendon aging.</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

HMGA2 Attenuates Tendon Stem/Progenitor Cell Senescence Via PI3K/AKT-Mediated Mitophagy Activation and SASP Suppression

  • 期刊论文

  • 发表日期：

    2025年6月20日

查看全文
  • Hao Wang,
  • Guang-Chun Dai,
  • Yu-Cheng Gao,
  • Xiao-Yu Liu,
  • Pan-Pan Lu,
  • Mu-Min Cao,
  • Ren-Wang Sheng,
  • Liu Shi,
  • Zhang Cheng,
  • Ying-Juan Li,
  • Yun-Feng Rui

摘要

Tendon stem/progenitor cell (TSPC) senescence contributes to age-related tendon degeneration, yet the molecular mechanisms underlying this process remain poorly understood. In present study, we investigated the role of High-Mobility Group A2 (HMGA2) in TSPCs senescence. During the tendon aging, we showed that HMGA2 expression decreases with age. In senescent TSPCs, HMGA2 overexpression significantly delayed TSPCs senescence. Additionally, overexpression of HMGA2 restored the age-related dysfunction of migration, tenogenic differentiation, and mitophagy. HMGA2 also suppressed the senescence-associated secretory phenotype (SASP), downregulating inflammatory cytokines such as IL-1β, IL-6, and TGF-β. Furthermore, we suggested that the PI3K-AKT signaling pathway is activated in senescent TSPCs, and HMGA2 overexpression could inhibit the PI3K-AKT signaling pathway activation, which demonstrates that HMGA2 might attenuate senescence and age-related dysfunction of TSPCs through the repression of PI3K-AKT signaling pathway. Our findings collectively indicated the crucial involvement of HMGA2 in TSPCs senescence regulation and suggested a novel target for preventing tendon aging.