ReviewFrontiers in immunology2026
The role of extracellular matrix stiffness in regulating fibroblast behaviors and disease progression.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
As a representative physical factor in the extracellular matrix (ECM), ECM stiffness regulates fibroblast behaviors and contributes to physiological homeostasis and pathological processes. This process relies on mechanosensors, including integrin-based adhesion complexes, mechanosensitive ion channels, and discoidin domain receptors (DDRs), which detect changes in stiffness and transduce them into biochemical signals. Through downstream pathways including YAP/TAZ and RhoA/ROCK, ECM stiffness modulates essential cellular behaviors such as adhesion, migration, proliferation, and differentiation, adapting to the requirements of tissue homeostasis. Under pathological conditions, abnormal elevation of ECM stiffness occurs in tumor and fibrotic tissues, forming a vicious cycle of ECM deposition-increased stiffness-abnormal cellular activation. Therefore, deciphering the regulatory mechanisms of ECM stiffness on fibroblasts not only deepens the understanding of the interaction between cells and the mechanical microenvironment but also provides crucial theoretical support and innovative ideas for the targeted therapy of diseases such as tumors and fibrosis, as well as the development of tissue engineering and regenerative medicine.
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