DAMP: bridging mechanotransduction and immune responses in tendinopathy
- 1Shenzhen Key Laboratory of Systems Medicine for Inflammatory Diseases, Zhongshan School of Medicine, Sun Yat-sen University, Sun Yat-Sen University
- 2Department of Orthopedics, Zhongshan Hospital of Traditional Chinese Medicine Affiliated to Guangzhou University of Traditional Chinese Medicine
Abstract
Tendinopathy is increasingly recognized as a chronic degenerative disorder driven by sterile inflammation, where persistent mechanical stress and dysregulated innate immunity converge to disrupt tissue homeostasis. Damage-associated molecular patterns (DAMPs), released from stressed or injured tenocytes and resident immune cells, serve as key mediators translating mechanical overload into sustained inflammatory responses. Their persistent release perpetuates inflammation, extracellular matrix disorganization, and impaired tissue repair, thereby establishing a self-sustaining cycle of degeneration. Recent studies have highlighted DAMPs as central regulators in the initiation and maintenance of tendon inflammation, reflecting an intricate interplay between mechanical cues, metabolic stress, and immune dysfunction. This review summarizes current understanding of DAMP-mediated mechanisms in tendinopathy, emphasizing their roles in inflammation, fibrosis, and tissue remodeling. We also discuss the therapeutic implications of modulating DAMP-driven signaling pathways to restore immune homeostasis and promote regenerative healing. A clearer understanding of these immunomechanical interactions provides a foundational framework for developing mechanism-based treatments that target the underlying causes of tendinopathy.
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BibTeX
@article{zheng2026damp,
title = {{DAMP: bridging mechanotransduction and immune responses in tendinopathy}},
author = {Hongjun Zheng and Shihua Gao and Zhuangfeng Weng},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1910397},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1910397/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - DAMP: bridging mechanotransduction and immune responses in tendinopathy
AU - Hongjun Zheng
AU - Shihua Gao
AU - Zhuangfeng Weng
PY - 2026
DA - 2026/10/14
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1910397
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1910397/full
AB - Tendinopathy is increasingly recognized as a chronic degenerative disorder driven by sterile inflammation, where persistent mechanical stress and dysregulated innate immunity converge to disrupt tissue homeostasis. Damage-associated molecular patterns (DAMPs), released from stressed or injured tenocytes and resident immune cells, serve as key mediators translating mechanical overload into sustained inflammatory responses. Their persistent release perpetuates inflammation, extracellular matrix disorganization, and impaired tissue repair, thereby establishing a self-sustaining cycle of degeneration. Recent studies have highlighted DAMPs as central regulators in the initiation and maintenance of tendon inflammation, reflecting an intricate interplay between mechanical cues, metabolic stress, and immune dysfunction. This review summarizes current understanding of DAMP-mediated mechanisms in tendinopathy, emphasizing their roles in inflammation, fibrosis, and tissue remodeling. We also discuss the therapeutic implications of modulating DAMP-driven signaling pathways to restore immune homeostasis and promote regenerative healing. A clearer understanding of these immunomechanical interactions provides a foundational framework for developing mechanism-based treatments that target the underlying causes of tendinopathy.
SN - 1664-3224
ER -