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Lineage\u2010tracing and single\u2010cell studies reveal that matrifibrocytes arise from activated myofibroblasts during late scar maturation, lose\n                    <jats:italic>\u03b1<\/jats:italic>\n                    \u2010SMA and proliferative capacity, and adopt a cartilage\u2010like ECM program (e.g.,\n                    <jats:italic>Comp<\/jats:italic>\n                    ,\n                    <jats:italic>Chad<\/jats:italic>\n                    ,\n                    <jats:italic>Thbs4<\/jats:italic>\n                    ,\n                    <jats:italic>Sfrp2<\/jats:italic>\n                    ). Functionally, they stabilize collagen architecture, sustain tensile strength and shape an immune\u2010quiescent, angiogenesis\u2010restrained microenvironment. We synthesize evidence suggesting that TGF\u2010\n                    <jats:italic>\u03b2<\/jats:italic>\n                    restraint (e.g.,\n                    <jats:italic>Smad7<\/jats:italic>\n                    ), matrix mechanics (YAP\/TAZ), Wnt attenuation (\n                    <jats:italic>Sfrp2<\/jats:italic>\n                    ),\n                    <jats:italic>Comp\u2013Notch3<\/jats:italic>\n                    feedback, and\n                    <jats:italic>Thbs4\u2013Atf6\u03b1<\/jats:italic>\n                    ER\u2010stress adaptation converge to establish or maintain this terminal state. We further summarize disease contexts beyond infarction, including pressure overload and valvular disease, where matrifibrocyte\u2010like programs emerge and may contribute to chronic stiffening. Finally, we outline translational strategies that either accelerate matrifibrocyte maturation to secure scars after acute injury or reset terminal states via pharmacology or direct reprogramming to regress fibrosis. Framing matrifibrocytes as an adjustable endpoint reconciles structural integrity with functional recovery and highlights actionable checkpoints for precision anti\u2010fibrotic therapy.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.71174","type":"journal-article","created":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T04:15:13Z","timestamp":1778732113000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Matrifibrocytes Redefine Cardiac Fibrosis: From Terminal Differentiation to Translational Modulation"],"prefix":"10.1111","volume":"30","author":[{"given":"Zhentao","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Surgery, Davis Heart and Lung Research Institute The Ohio State University Wexner Medical Center  Columbus Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hua","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of 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