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The hallmark pathological feature of excessive extracellular matrix (ECM) deposition severely undermines the efficacy of mesenchymal stem cell (MSC)\u2010based treatments. While existing MSC therapeutic strategies primarily focus on modulating inflammation in early stages, they have not yet established precise interventions addressing the core pathological mechanism\u2014ECM dysregulation. Previous studies demonstrated the therapeutic potential of human embryonic stem cell (hESCs)\u2010derived immunity\u2010and\u2010matrix\u2010regulatory cells (IMRCs) in lung injury and fibrosis models. However, the critical biomarkers and underlying mechanisms mediating IMRCs' efficacy in IPF remain poorly understood. In this study, we generated\n                    <jats:italic>MMP1<\/jats:italic>\n                    knockout IMRCs (IMRCs\u2010\n                    <jats:italic>MMP1 KO<\/jats:italic>\n                    ) using CRISPR\u2010based gene editing. We then characterized whether MMP1 ablation affected key properties of IMRCs, including cell morphology, proliferation, migration, marker protein expression, transcriptomic profile, and cytokine secretion. Subsequently, the ability of IMRCs\u2010\n                    <jats:italic>MMP1 KO<\/jats:italic>\n                    to degrade collagen was tested using in\u00a0vivo and in\u00a0vitro pulmonary fibrosis models.\n                    <jats:italic>MMP1<\/jats:italic>\n                    knockout was successfully achieved and did not compromise typical IMRC characteristics or impair their immunomodulatory capacity. However, MMP1 deficiency significantly attenuated the ability of IMRCs to degrade TGF\u2010\u03b21\u2010induced collagen I deposition in A549 cells. Importantly, wild\u2010type IMRCs demonstrated superior therapeutic efficacy in ameliorating bleomycin\u2010induced lung injury and fibrosis in mice compared with IMRCs\u2010\n                    <jats:italic>MMP1 KO<\/jats:italic>\n                    . Furthermore, IMRCs exhibited significantly greater capability to directly degrade the pericellular collagen I and modulate fibroblasts' activation progression within fibrotic lung tissues in a MMP1\u2010dependent manner. In summary, our data establish that MMP1 plays an essential functional role in IMRC\u2010mediated attenuation of PF. MMP1 thus represents a key therapeutic biomarker for IMRC\u2010based treatment. This work provides a foundation for developing stem cell therapies tailored to the pathological features of IPF, potentially enabling adaptive treatment strategies.\n                  <\/jats:p>","DOI":"10.1111\/cpr.70267","type":"journal-article","created":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T07:34:54Z","timestamp":1785915294000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Human Embryonic Stem Cell\u2010Derived Immunity\u2010And\u2010Matrix\u2010Regulatory Cells Attenuate Pulmonary Fibrosis via\n                    <scp>MMP1<\/scp>\n                    \u2010Mediated Collagen Degradation"],"prefix":"10.1111","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9137-9519","authenticated-orcid":false,"given":"Zhongwen","family":"Li","sequence":"first","affiliation":[{"name":"State Key Laboratory of Organ Regeneration and Reconstruction Institute of Zoology, Chinese Academy of Sciences  Beijing China"},{"name":"Beijing Institute for Stem Cell and Regenerative Medicine  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dingyun","family":"Song","sequence":"additional","affiliation":[{"name":"Senior Department of Respiratory and Critical Care Medicine The Eighth Medical Center of Chinese PLA General Hospital  Beijing China"},{"name":"National Center for Respiratory Medicine; 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