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REVIEW article

Front. Endocrinol.

Sec. Diabetes: Molecular Mechanisms

Volume 16 - 2025 | doi: 10.3389/fendo.2025.1551853

Treatment of T2DM-related inflammation and vascular injury by regulating cellular crosstalk in the islet microenvironment

Provisionally accepted
  • 1Changchun University of Chinese Medicine, Changchun, China
  • 2Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, Beijing Municipality, China
  • 3Beijing University of Chinese Medicine, Beijing, Beijing Municipality, China
  • 4Guang'anmen Hospital South Campus, Guang’anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, Beijing Municipality, China

The final, formatted version of the article will be published soon.

Type 2 diabetes mellitus (T2DM), a complex systemic metabolic disorder caused by multiple factors, has been linked to numerous acute and chronic complications. T2DM pathogenesis includes glucotoxicity, lipotoxicity, inflammatory cytokines, and amyloid formation. Within the pancreatic islet microenvironment, the crosstalk among cell types plays a significant role in these pathogenic mechanisms. Islet β cells, macrophages, and endothelial cells, the three primary cell types, engage in intercellular communication under physiological and pathological conditions, critical to maintaining islet homeostasis and promoting the pathological progression of T2DM. This review discusses the interactions between these islet cells, particularly how their crosstalk affects islet function and T2DM development. Additionally, natural products targeting islet cell interactions are discussed as a therapeutic approach for T2DM, along with other personalized treatment options, including exosomes, parasitic therapy, and dietary interventions. Emerging strategies that regulate intercellular signaling and complex crosstalk within the islet microenvironment offer promising avenues for T2DM treatment.

Keywords: type 2 diabetes mellitus, Islet microenvironment, cellular crosstalk, Natural Products, therapy

Received: 26 Dec 2024; Accepted: 24 Sep 2025.

Copyright: © 2025 Sun, Yang, Sun, Zhou, Luo, Bao, Tong, Lin and Han. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Xiaolin Tong, tongxiaolin@vip.163.com
Yiqun Lin, 84289959@qq.com
Lin Han, hanlin_med@163.com

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.