Special Issues

Special Issue Title: Cardiac fibrosis

· Print Special Issue Flyer

· Deadline for manuscript submissions:  1 June 2020 

Special Issue Editor

Guest Editor

Prof. Dr. Ian M.C. Dixon

Department of Physiology and Pathophysiology, Institute of Cardiovascular Sciences, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada

Website | E-Mail

Interests: Studying the signals that regulate fibroblast activation and deactivation in heart failure and in normal heart.  We specialize in proteins such as SKI, a known fibroblast deactivator, as well as in how matrix substrate stiffness provides input to regulate fibroblast phenotype.

Prof. Dr. Onur Kanisicak

Division of Regenerative Medicine, Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, USA

Website | E-Mail

Interests: The examination and manipulation of various cellular compartments within the cardiovascular and musculoskeletal system with an overall goal to identify novel therapeutic targets to prevent fibrosis and promote wound healing. Towards these efforts, current projects in the Kanisicak lab employ in vivo genetic interrogation methods to determine the lineage plasticity and role of tissue-resident interstitial cells involved in fibrogenesis, regeneration, and angiogenesis.

Special Issue Information

Dear Colleagues,

For the past decade, investigation on the causes that underpin cardiac fibrosis has created its own niche in the literature. Fibrosis occurs not only in the myocardium but is important in consideration of the pathogenesis of valvular diseases and vascular dysfunction. The level of interest in cardiac fibrosis is currently very high, and the number of laboratories involved in the investigation of this disease state is burgeoning especially as it is now widely recognized that fibrosis of the heart per se is a common independent cause for cardiac muscle dysfunction. Nonetheless we are no nearer to finding a clinical solution for the inappropriate activation of fibroblasts or small molecule inhibitor to quell generalized cardiac dysfunction that is associated with the dysregulation and expansion of the cardiac interstitium, than we were 10 years ago. A major consideration of the complexity in seeking a universally effective anti-fibrotic agent is that the phenotype and behaviour of fibroblasts residing in different organs are themselves different from one another. Not to mention the distinct fibroblast activity and their cellular fate during various disease states in the heart. Thus the investigator would do well to consider the specific source organ (heart, lung, artery), type of disease, or even of specific structures or topographical origins of fibroblasts within a given organ e.g., cardiac valves, or atrial vs ventricular-sourced fibroblasts when investigating specific fibrotic processes. In this sense, perhaps it is an ideal point in the history of development of the main ideas surrounding the pathogenesis fibrotic processes to ask questions about the activation of quiescent fibroblasts to myofibroblasts, so as to provide clues as to the key triggers of cellular events that underpin tissue fibrosis. Further, as tissues are a complex arrangement of various cell types, researchers would be well-served to pose hypotheses that address cell-to-cell crosstalk, and matrix-to-cell signals. Recent developments in the literature reveal that progenitor cells and key players in the immune response may be at the basis of control of activation of fibroblasts, and the purpose of this book will be to highlight the latest developments in these areas, so as to develop a rational approach to quelling fibroblast activation and consequential degradation of tissue performance that is associated with generalized fibrosis.

Prof. Dr. Ian M.C. Dixon and Prof. Dr. Onur Kanisicak

Guest Editors


Manuscript Submission Information

Manuscripts should be submitted online at https://rcm.imrpress.org 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 double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Reviews in Cardiovascular Medicine is an international peer-reviewed open access quarterly journal published by IMR Press.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is $1950. Submitted papers should be well formatted and use good English.


Fibroblast; Myofibroblast; Extracellular matrix; Tissue fibrosis; Cardiac fibrosis; Fibrillogenesis; Cellular cross-talk; Inflammation; Cell fate; Biomechanical signaling

Share This Special Issue


Please wait a minute...
For Selected: Toggle Thumbnails
Cardiac sarcoidosis: diagnosis and management
Eleftherios Markatis, Andreas Afthinos, Emmanouil Antonakis, Ilias C Papanikolaou
Reviews in Cardiovascular Medicine    2020, 21 (3): 321-338.   DOI: 10.31083/j.rcm.2020.03.102
Abstract1879)   HTML365)    PDF(pc) (886KB)(2104)       Save

Sarcoidosis is a chronic inflammatory disease of unknown etiology characterized by multi-organ involvement. End-organ disease consists of granulomatous inflammation, which if left untreated or not resolved spontaneously, leads to permanent fibrosis and end-organ dysfunction. Cardiac involvement and fibrosis in sarcoidosis occur in 5-10% of cases and is becoming increasingly diagnosed. This is due to increased clinical awareness among clinicians and new diagnostic modalities, since magnetic resonance imaging and positron-emission tomography are emerging as “gold standard” tools replacing endomyocardial biopsy. Despite this progress, isolated cardiac sarcoidosis is difficult to differentiate from other causes of arrhythmogenic cardiomyopathy. Cardiac fibrosis leads to congestive heart failure, arrhythmias and sudden cardiac death. Immunosuppressives (mostly corticosteroids) are used for the treatment of cardiac sarcoidosis. Implantable devices like a cardioverter-defibrillator may be warranted in order to prevent sudden cardiac death. In this article current trends in the pathophysiology, diagnosis and management of cardiac sarcoidosis will be reviewed focusing on published research and latest guidelines. Lastly, a management algorithm is proposed.

Table and Figures | Reference | Related Articles | Metrics

Current Issue

  • Volume 22, Issue 3