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<p>Tendinopathy, characterized by persistent pain and impaired function, is a globally prevalent condition imposing heavy socioeconomic burdens. Long regarded as an isolated local lesion, it is increasingly recognized as a regional manifestation of systemic dysregulation driven by the metabolic-endocrine-aging axis—not merely a peripheral “background factor.” This review systematically analyzes four key pathogenic pathways: hyperglycemia-induced advanced glycation end-product (AGE) deposition, dyslipidemia-driven metabolic inflammation, sex hormone fluctuation-mediated collagen homeostasis disruption, and the cellular senescence-senescence-associated secretory phenotype (SASP) cascade. Together, these systemic factors remodel the tendon cell microenvironment, alter extracellular matrix biomechanics, and reduce the tissue’s mechanical load tolerance. Traditional local-focused treatments have demonstrated limited efficacy, requiring a shift to a “systemic-local synergistic regulation” paradigm. Critically, a new clinical staging system integrating systemic risk factors is urgently needed. By establishing a “systemic-local” crosstalk model and highlighting the urgent need for a novel clinical staging system integrating systemic risk factors—our primary novel contribution—this review provides key insights for researchers and clinicians, supporting the optimization of personalized therapeutic strategies and improved clinical outcomes for tendinopathy.</p>

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Beyond local injury: pathogenic roles of metabolic, endocrine, and aging-associated systemic factors in tendinopathy and novel therapeutic strategies

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月27日

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  • Yuqi Lin,
  • Zhichao Liu,
  • Lianjie Peng,
  • Shihan Wang,
  • Kun Li,
  • Xingyu Lv,
  • Jianxiang He

摘要

Tendinopathy, characterized by persistent pain and impaired function, is a globally prevalent condition imposing heavy socioeconomic burdens. Long regarded as an isolated local lesion, it is increasingly recognized as a regional manifestation of systemic dysregulation driven by the metabolic-endocrine-aging axis—not merely a peripheral “background factor.” This review systematically analyzes four key pathogenic pathways: hyperglycemia-induced advanced glycation end-product (AGE) deposition, dyslipidemia-driven metabolic inflammation, sex hormone fluctuation-mediated collagen homeostasis disruption, and the cellular senescence-senescence-associated secretory phenotype (SASP) cascade. Together, these systemic factors remodel the tendon cell microenvironment, alter extracellular matrix biomechanics, and reduce the tissue’s mechanical load tolerance. Traditional local-focused treatments have demonstrated limited efficacy, requiring a shift to a “systemic-local synergistic regulation” paradigm. Critically, a new clinical staging system integrating systemic risk factors is urgently needed. By establishing a “systemic-local” crosstalk model and highlighting the urgent need for a novel clinical staging system integrating systemic risk factors—our primary novel contribution—this review provides key insights for researchers and clinicians, supporting the optimization of personalized therapeutic strategies and improved clinical outcomes for tendinopathy.