Resident cardiac macrophages: crucial modulators of cardiac (patho)physiology
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REVIEW
Resident cardiac macrophages: crucial modulators of cardiac (patho) physiology M. Sansonetti1 · F. J. G. Waleczek1 · M. Jung1 · T. Thum1,2 · F. Perbellini1 Received: 24 September 2020 / Accepted: 23 November 2020 © The Author(s) 2020
Abstract Resident cardiac macrophages (rcMacs) are integral components of the myocardium where they have key roles for tissue homeostasis and in response to inflammation, tissue injury and remodelling. In this review, we summarize the current knowledge and limitations associated with the rcMacs studies. We describe their specific role and contribution in various processes such as electrical conduction, efferocytosis, inflammation, tissue development, remodelling and regeneration in both the healthy and the disease state. We also outline research challenges and technical complications associated with rcMac research. Recent technological developments and contemporary immunological techniques are now offering new opportunities to investigate the separate contribution of rcMac in respect to recruited monocytes and other cardiac cells. Finally, we discuss new therapeutic strategies, such as drugs or non-coding RNAs, which can influence rcMac phenotype and their response to inflammation. These novel approaches will allow for a deeper understanding of this cardiac endogenous cell type and might lead to the development of more specific and effective therapeutic strategies to boost the heart’s intrinsic reparative capacity. Keywords Inflammation · Phagocytes · Macrophages · Resident cells
Introduction For several decades, bone marrow-derived macrophages were considered as the only large phagocytes involved in homeostasis, tissue healing, and defence against pathogens. Emerging evidence has overturned this dogma and has shown that resident macrophages (rMacs) are also fundamental players in a plethora of functions and cellular interactions both in homeostasis and in the modulation of the inflammatory response following injury and in tissue remodelling. Originating from the yolk sac or fetal liver progenitors [45], tissue rMacs inhabit various organs such as the bone marrow [58], lungs [76], liver [12], pancreas [17], brain [96], and heart [34]. Differently from circulating * T. Thum Thum.Thomas@mh‑hannover.de * F. Perbellini Perbellini.Filippo@mh‑hannover.de 1
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany
Fraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany
2
immune cells, rMac retain tissue-specific features. This population is made up of macrophages ontogenetically older than bone marrow-derived macrophages [95], they are evolutionarily conserved [30] and present throughout the lifetime. They can proliferate in situ and this process is exacerbated during inflammation [41]. In murine cardiac tissue, resident cardiac macrophages (rcMac) are reported to constitute up to 5–10% of the non-myocyte population, a percentage that increases dramatically following cardiac damage [50, 89]
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