{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T12:31:22Z","timestamp":1789561882976,"version":"build-2803163510"},"reference-count":227,"publisher":"MDPI AG","issue":"19","license":[{"start":{"date-parts":[[2020,9,28]],"date-time":"2020-09-28T00:00:00Z","timestamp":1601251200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Fondo di Ateneo per la Ricerca FAR 2018","award":["N\/A"],"award-info":[{"award-number":["N\/A"]}]},{"name":"Fondo di Ateneo per la Ricerca FAR 2019","award":["N\/A"],"award-info":[{"award-number":["N\/A"]}]},{"DOI":"10.13039\/501100005010","name":"Associazione Italiana per la Ricerca sul Cancro","doi-asserted-by":"publisher","award":["MFAG 2019-ID 22818"],"award-info":[{"award-number":["MFAG 2019-ID 22818"]}],"id":[{"id":"10.13039\/501100005010","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002803","name":"Fondazione Cariplo","doi-asserted-by":"publisher","award":["ID 2019-1609"],"award-info":[{"award-number":["ID 2019-1609"]}],"id":[{"id":"10.13039\/501100002803","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Ministero della Salute_Ricerca Corrente_IRCCS MultiMeidca","award":["N\/A"],"award-info":[{"award-number":["N\/A"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Despite relevant advances made in therapies for cardiovascular diseases (CVDs), they still represent the first cause of death worldwide. Cardiac fibrosis and excessive extracellular matrix (ECM) remodeling are common end-organ features in diseased hearts, leading to tissue stiffness, impaired myocardial functional, and progression to heart failure. Although fibrosis has been largely recognized to accompany and complicate various CVDs, events and mechanisms driving and governing fibrosis are still not entirely elucidated, and clinical interventions targeting cardiac fibrosis are not yet available. Immune cell types, both from innate and adaptive immunity, are involved not just in the classical response to pathogens, but they take an active part in \u201csterile\u201d inflammation, in response to ischemia and other forms of injury. In this context, different cell types infiltrate the injured heart and release distinct pro-inflammatory cytokines that initiate the fibrotic response by triggering myofibroblast activation. The complex interplay between immune cells, fibroblasts, and other non-immune\/host-derived cells is now considered as the major driving force of cardiac fibrosis. Here, we review and discuss the contribution of inflammatory cells of innate immunity, including neutrophils, macrophages, natural killer cells, eosinophils and mast cells, in modulating the myocardial microenvironment, by orchestrating the fibrogenic process in response to tissue injury. A better understanding of the time frame, sequences of events during immune cells infiltration, and their action in the injured inflammatory heart environment, may provide a rationale to design new and more efficacious therapeutic interventions to reduce cardiac fibrosis.<\/jats:p>","DOI":"10.3390\/ijms21197165","type":"journal-article","created":{"date-parts":[[2020,9,28]],"date-time":"2020-09-28T10:39:58Z","timestamp":1601289598000},"page":"7165","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":68,"title":["Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis"],"prefix":"10.3390","volume":"21","author":[{"given":"Denisa","family":"Baci","sequence":"first","affiliation":[{"name":"Immunology and General Pathology Laboratory, Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5027-880X","authenticated-orcid":false,"given":"Annalisa","family":"Bosi","sequence":"additional","affiliation":[{"name":"Laboratory of Pharmacology, Department of Medicine and Surgery, University of Insubria, 21100 Varese, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3511-7992","authenticated-orcid":false,"given":"Luca","family":"Parisi","sequence":"additional","affiliation":[{"name":"Department of Biomedical, Surgical and Dental Sciences, School of Dentistry, University of Milan, 20122 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2881-720X","authenticated-orcid":false,"given":"Giuseppe","family":"Buono","sequence":"additional","affiliation":[{"name":"Unit of Immunology, IRCCS MultiMedica, 20138 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4757-7101","authenticated-orcid":false,"given":"Lorenzo","family":"Mortara","sequence":"additional","affiliation":[{"name":"Immunology and General Pathology Laboratory, Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giuseppe","family":"Ambrosio","sequence":"additional","affiliation":[{"name":"Division of Cardiology, University of Perugia School of Medicine, 06123 Perugia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4790-0861","authenticated-orcid":false,"given":"Antonino","family":"Bruno","sequence":"additional","affiliation":[{"name":"Unit of Immunology, IRCCS MultiMedica, 20138 Milan, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2020,9,28]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"74","DOI":"10.1038\/s41569-018-0144-3","article-title":"Targeting inflammation in CVD: Advances and challenges","volume":"16","author":"Moore","year":"2019","journal-title":"Nat. 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