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In mammalian tissues, sterile tissue injury activates a suite of stress\u2010activated programs that integrate cytoprotective stress responses that are tightly coupled with carefully regulated and precisely timed inflammatory signaling, thereby promoting tissue repair while simultaneously limiting collateral damage. Although the terminology for this phenomenon is still evolving, the recently described concept of \u201cdisease tolerance\u201d has been proposed to explain tissue\u2010intrinsic cell autonomous molecular programs that couple cytoprotective stress responses with tightly regulated inflammatory signaling that minimizes collateral damage while also activating tissue repair mechanisms. Emerging evidence reviewed here suggests that sterile cardiac injury (e.g., myocardial ischemia or hemodynamic pressure overload) elicits an acquired stress\u2010tolerant state that sustains cytoprotective programs in cardiac myocytes and constrains collateral immune\u2010mediated tissue injury. However, these stress\u2010activated pathways are highly context\u2010dependent and are shaped by the magnitude and duration of the ensuing inflammatory response. When tissue injury\u2010induced inflammation is sustained and\/or excessive, it can also lead to unwanted collateral tissue damage and cardiac decompensation.<\/jats:p>","DOI":"10.1111\/imr.70126","type":"journal-article","created":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T05:19:18Z","timestamp":1777439958000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["In Defense of Homeostasis: Innate Immunity in Cardiac Injury and Repair"],"prefix":"10.1111","volume":"339","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2516-0145","authenticated-orcid":false,"given":"Douglas L.","family":"Mann","sequence":"first","affiliation":[{"name":"Center for Cardiovascular Research, Cardiovascular Division Washington University School of Medicine  St. Louis Missouri 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