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Purpose of Review <p>This review aims to summarize current knowledge of the alterations and pathophysiological roles of adipose tissue (AT)-derived extracellular vesicles (AT-EVs) and adipocyte-derived EVs (Ad-EVs) in the context of obesity, while providing mechanistic insights into their potential functions within the tumor microenvironment.</p> Recent Findings <p>Emerging evidence indicates that obese AT-EVs and Ad-EVs contribute to insulin resistance, diabetes, metabolic dysfunction-associated steatotic liver disease, cardiovascular disorders, and cancer by delivering pathological cargo or altering recipient cell signaling. Conversely, both lean and obese AT-EVs and Ad-EVs have demonstrated therapeutic potential in specific settings, such as restoring insulin sensitivity, enhancing β-cell function, improving wound healing, and mitigating ischemia/reperfusion injury.</p> Summary <p>One of the most prominent features of obesity is AT remodeling, which&#xa0;markedly increases the release of EVs and alters their cargo composition. These EVs can&#xa0;play context-dependent roles in pathophysiological processes, underscoring the&#xa0;complexity of AT-EV and Ad-EV biology and highlighting the need for further mechanistic&#xa0;investigations, particularly in cancer, where evidence remains limited. Advancing our&#xa0;understanding of the molecular pathways underlying their biogenesis, cargo sorting, and&#xa0;intercellular communication will not only deepen our knowledge of obesity-related&#xa0;pathophysiology but also facilitate the development of novel biomarkers and EV-based&#xa0;therapeutic strategies.</p>

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Pathophysiological Roles of Obesity-Induced Alterations in Extracellular Vesicles Derived from Adipose Tissue and Adipocytes

  • 期刊论文

  • 发表日期：

    2026年1月16日

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  • Inae Jeong,
  • Ok-Kyung Kim

摘要

Purpose of Review

This review aims to summarize current knowledge of the alterations and pathophysiological roles of adipose tissue (AT)-derived extracellular vesicles (AT-EVs) and adipocyte-derived EVs (Ad-EVs) in the context of obesity, while providing mechanistic insights into their potential functions within the tumor microenvironment.

Recent Findings

Emerging evidence indicates that obese AT-EVs and Ad-EVs contribute to insulin resistance, diabetes, metabolic dysfunction-associated steatotic liver disease, cardiovascular disorders, and cancer by delivering pathological cargo or altering recipient cell signaling. Conversely, both lean and obese AT-EVs and Ad-EVs have demonstrated therapeutic potential in specific settings, such as restoring insulin sensitivity, enhancing β-cell function, improving wound healing, and mitigating ischemia/reperfusion injury.

Summary

One of the most prominent features of obesity is AT remodeling, which markedly increases the release of EVs and alters their cargo composition. These EVs can play context-dependent roles in pathophysiological processes, underscoring the complexity of AT-EV and Ad-EV biology and highlighting the need for further mechanistic investigations, particularly in cancer, where evidence remains limited. Advancing our understanding of the molecular pathways underlying their biogenesis, cargo sorting, and intercellular communication will not only deepen our knowledge of obesity-related pathophysiology but also facilitate the development of novel biomarkers and EV-based therapeutic strategies.