{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T11:14:58Z","timestamp":1790248498910,"version":"4.1.0"},"reference-count":183,"publisher":"The Company of Biologists","issue":"18","funder":[{"name":"University of California, San Francisco","id":[{"id":"https:\/\/ror.org\/043mz5j54","id-type":"ROR","asserted-by":"crossref"}]},{"name":"Edward Mallinckrodt, Jr. Foundation","id":[{"id":"https:\/\/ror.org\/035yf7a66","id-type":"ROR","asserted-by":"crossref"}]},{"name":"Larry L. Hillblom Foundation","id":[{"id":"https:\/\/ror.org\/00br6vq85","id-type":"ROR","asserted-by":"crossref"}]},{"name":"American Federation for Aging Research","id":[{"id":"https:\/\/ror.org\/000r61a05","id-type":"ROR","asserted-by":"crossref"}]},{"name":"California Institute for Regenerative Medicine","id":[{"id":"https:\/\/ror.org\/033m8b439","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Aging tissues paradoxically stiffen while losing mechanical resilience, becoming fragile, poorly regenerative and chronically inflamed. We review evidence that these phenotypes emerge from progressive failure of mechanotransduction across a mechanically integrated axis linking extracellular matrix (ECM) architecture, integrin adhesions, cytoskeletal force transmission and nuclear mechanics. We discuss how matrisome remodeling, glycation-driven crosslinking and reduced ECM turnover alter not only bulk stiffness but also fiber deformability, ligand presentation and matrix remodelability, thereby lowering the fidelity of mechanosensing. We then synthesize how distorted mechanical inputs and age-intrinsic changes in mechanotransduction machinery propagate through focal adhesion signaling, actin\u2013microtubule dynamics, mechanosensitive ion channels and nucleo-cytoskeletal coupling to dysregulate mechanosensitive transcription factors (including YAP\/TAZ and MRTF), promote senescence and amplify the senescence-associated secretory phenotype (SASP), which further degrades the ECM. Finally, we highlight premature aging syndromes as causal evidence showing that disruption of either ECM structure or nuclear integrity can collapse mechanotransductive homeostasis and trigger tissue degeneration. Together, these studies support a mechanical drift framework and motivate rejuvenation strategies aimed at resetting the aged mechanochemical niche.<\/jats:p>","DOI":"10.1242\/jcs.264835","type":"journal-article","created":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T10:48:09Z","timestamp":1790246889000},"source":"Crossref","is-referenced-by-count":0,"title":["The mechanisms and mechanics of aging"],"prefix":"10.1242","volume":"139","author":[{"given":"Anastasia","family":"Zhurikhina","sequence":"first","affiliation":[{"name":"University of California, San Francisco 1 Department of Biochemistry and Biophysics , , San Francisco, CA 94158 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-9806-1882","authenticated-orcid":false,"given":"Maia","family":"Kirkegaard","sequence":"additional","affiliation":[{"name":"University of California, San Francisco 2 Tetrad Graduate Program , , San Francisco, CA 94158 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4546-0775","authenticated-orcid":false,"given":"Alberto","family":"Guarnieri","sequence":"additional","affiliation":[{"name":"Genentech 3 , South San Francisco, CA 94080 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8910-1999","authenticated-orcid":false,"given":"Hanna L.","family":"Martens","sequence":"additional","affiliation":[{"name":"University of California, San Francisco 1 Department of Biochemistry and Biophysics , , San Francisco, CA 94158 ,","place":["USA"]},{"name":"Freeman Hrabowski Scholar 4 , Howard Hughes Medical Institute, Chevy Chase, MD 20815-6789 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2026,9,24]]},"reference":[{"key":"2026092406480024100_JCS264835C1","doi-asserted-by":"publisher","first-page":"eaat8657","DOI":"10.1126\/science.aat8657","article-title":"cGAS in action: expanding roles in immunity and inflammation","volume":"363","author":"Ablasser","year":"2019","journal-title":"Science"},{"key":"2026092406480024100_JCS264835C2","doi-asserted-by":"publisher","first-page":"107283","DOI":"10.1016\/j.isci.2023.107283","article-title":"A defective mechanosensing pathway affects fibroblast-to-myofibroblast transition in the old male mouse heart","volume":"26","author":"Angelini","year":"2023","journal-title":"iScience"},{"key":"2026092406480024100_JCS264835C3","doi-asserted-by":"publisher","first-page":"8285","DOI":"10.3390\/ijms24098285","article-title":"3D ECM-based scaffolds boost young cell secretome-derived EV rejuvenating effects in senescent cells","volume":"24","author":"Arcuri","year":"2023","journal-title":"Int. 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