{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T06:32:16Z","timestamp":1788849136453,"version":"build-2803163510"},"reference-count":177,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T00:00:00Z","timestamp":1786060800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:p>\n                    While mechanotransduction influences various lung cancer subtypes, this review focuses specifically on fibrosis-associated non-small cell lung cancer (NSCLC), where the progression from pulmonary fibrosis to malignancy is mediated by aberrant mechanotransduction. Progressive extracellular matrix (ECM) stiffening (8\u201325\u00a0kPa), mediated by lysyl oxidase (LOX)-dependent collagen crosslinking, establishes a \u201cmechano-immunological barrier.\u201d This barrier promotes malignant transformation and limits the efficacy of immunotherapy. Piezo1, a mechanically-activated cation channel, regulates this physical remodeling of the tumor microenvironment (TME). In the stiffened fibrotic stroma, mechanical tension activates Piezo1, causing intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx. This influx bypasses canonical Hippo signaling to activate the RCC2-YAP axis and induces \u201cepigenetic mechanical memory\u201d via Rho\/ROCK-mediated histone acetylation. Furthermore, Piezo1 modulates local immune responses. Mechanical stress activates Piezo1 in infiltrating T-cell, leading to epigenetic exhaustion and cytoskeletal impairment. Simultaneously, this mechanotransduction polarizes macrophages toward an immunosuppressive M2-like phenotype and mechanically induces PD-L1 expression on tumor cells. This review summarizes the Piezo1-mediated mechanotransduction networks involved in the fibrosis-to-cancer transition. We also discuss emerging \u201cmechano-immunotherapeutics,\u201d including targeted Piezo1 modulators, precision nanodelivery systems, and ECM-normalizing agents (e.g., LOX inhibitors and losartan). These strategies demonstrate synergistic effects when combined with immune checkpoint inhibitors. By softening the desmoplastic niche\u2014a tumor-associated microenvironment characterized by excessive fibrous connective tissue and a dense ECM\u2014and modulating mechanosensors, these interventions can convert immunosuppressive \u201ccold\u201d tumors into immunotherapy-responsive \u201chot\u201d microenvironments.\n                  <\/jats:p>","DOI":"10.3389\/fphar.2026.1845077","type":"journal-article","created":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T08:10:29Z","timestamp":1786090229000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["The mechano-immunological barrier in fibrosis-associated lung cancer: targeting matrix stiffness and the Piezo1 axis for microenvironment normalization"],"prefix":"10.3389","volume":"17","author":[{"given":"Linfeng","family":"Guo","sequence":"first","affiliation":[{"name":"Heilongjiang University of Chinese Medicine","place":["Harbin, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia","family":"Wang","sequence":"additional","affiliation":[{"name":"Hongqi Hospital of Mudanjiang Medical University","place":["Mudanjiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baoyi","family":"Ni","sequence":"additional","affiliation":[{"name":"Mudanjiang Medical University","place":["Mudanjiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiakang","family":"Jiang","sequence":"additional","affiliation":[{"name":"The First Affiliated Hospital of Heilongjiang University of Chinese Medicine","place":["Harbin, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,8,7]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"10204","DOI":"10.1038\/ncomms10204","article-title":"Epigenetic switch drives the conversion of fibroblasts into proinvasive cancer-associated fibroblasts","volume":"6","author":"Albrengues","year":"2015","journal-title":"Nat. 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