Special Issue "New Factors in Cell-Cell Communication between Monocyte/Macrophage and Cardiac Resident Cells during Cardiac Injury and Repair"

A special issue of Hearts (ISSN 2673-3846).

Deadline for manuscript submissions: 31 July 2021.

Special Issue Editors

Dr. Sören Meyer
E-Mail Website
Guest Editor
Department of Internal Medicine III, University Hospital Heidelberg, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany
Interests: inflammation; myocardial infarction; myocarditis; monocytes/macrophages; immunomodulation; Wnt signaling
Prof. Florian Leuschner
E-Mail Website
Guest Editor
Department of Internal Medicine III, University Hospital Heidelberg, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg/Mannheim, Heidelberg, Germany.
Interests: Immunocardiology; innate immunity; leukocyte kinetics; leukocyte activation

Special Issue Information

Dear Colleagues,

The innate immune response is the first line of defense that protects us from invading pathogens and infections. However, it is now well established that cells of the innate immunity also participate in sterile inflammation and tissue repair. Cells of the myeloid cell lineage, especially monocytes and macrophages, have been identified as crucial players in the healing myocardium.

In response to cardiac injury, cardiac resident macrophages proliferate, and high numbers of monocytes infiltrate the heart, where they interact with various cell types including cardiomyocytes, fibroblasts, and endothelial cells. Recent technical advances have revealed a tremendous plasticity and heterogeneity within the myeloid cell compartment in the injured heart. This is also reflected by the variety of tasks monocytes and macrophages fulfill during cardiac repair, ranging from the removal of dead cells and tissue debris, promoting angiogenesis, to coordinating extracellular matrix deposition. However, little is known about the factors released in the cardiac niche that guide monocyte/macrophage function and may coordinate monocyte/macrophage plasticity and heterogeneity.

This Special Issue is dedicated to research that advances our understanding of mechanisms and factors that play a role in cell-cell communication between cardiac resident cells and monocyte macrophages and determine their cellular fate and function during cardiac repair.

Dr. Sören Meyer
Prof. Florian Leuschner
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Hearts is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • Monocytes/Macrophages
  • inflammation
  • monocyte/macrophage differentiation
  • monocyte/macrophage heterogeneity
  • cell-cell communication
  • myocardial injury
  • cardiac remodeling

Published Papers

This special issue is now open for submission.
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