Key result
Immuno-instructive biomaterials can reshape the post-infarction microenvironment by steering macrophages toward reparative phenotypes.
Why the study?
Reperfusion for coronary artery disease and myocardial infarction does not sufficiently correct immune dysregulation or prevent adverse remodeling.
Immuno-instructive biomaterials represent a promising complementary strategy to reperfusion for improving tissue repair and preventing adverse remodeling after myocardial infarction.
May complement reperfusion in MI by targeting inflammation and remodeling; extends RCT evidence for localized biomaterial immunomodulation.
Coronary artery disease (CAD) and myocardial infarction (MI) feature a highly dynamic inflammatory milieu. While reperfusion remains essential, it does not sufficiently correct immune dysregulation or prevent adverse remodeling. Biomaterials offer a complementary strategy by enabling spatiotemporally controlled immunomodulation and tissue repair. By providing localized delivery of bioactive cues, mechanical support to stabilize the infarct wall, and immuno-instructive interfaces that steer macrophages toward reparative phenotypes, biomaterial platforms can reshape the post-infarction microenvironment. This review summarizes recent biomaterial-mediated strategies for the treatment of coronary heart disease. By integrating advances in immunomodulatory design, controlled drug delivery, and cardiac tissue engineering, it highlights how biomaterials can reshape the post-ischemic microenvironment to improve repair and limit adverse remodeling. These insights not only clarify current opportunities and translational barriers, but also provide guidance for developing next-generation, phase-adaptive and clinically scalable biomaterial platforms.
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Chi et al. (2026) conducted a review in Coronary artery disease and myocardial infarction. Immuno-instructive biomaterials was evaluated. Immuno-instructive biomaterials can reshape the post-infarction microenvironment by providing localized delivery of bioactive cues, mechanical support, and steering macrophages toward reparative phenotypes.
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