Cardiomyopathy: Pathogenesis, Diagnosis, and Treatment

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (15 July 2023) | Viewed by 3449

Special Issue Editor


E-Mail Website
Guest Editor
Centro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain
Interests: arrhythmogenic cardiomyopathy

Special Issue Information

Dear Colleagues,

Heart muscle disease, a leading cause of death worldwide, is etiologically and phenotypically heterogeneous and is caused by a combination of genetic and non-genetic factors. Cardiomyopathies are defined as myocardial disorders in which the heart is structurally or/and functionally abnormal. Recent progress in elucidating molecular, cellular and physiological mechanisms has promoted new concepts that have inspired more effective treatment strategies. This special issue on Cardiomyopathies Pathogenesis, Diagnosis, and Treatment will focus on the fundamental mechanisms that drive genetic and SARS-Cov2 induced cardiomyopathies, with the main goal of uncovering novel pathways and targets to predict the development of the disease and to protect or restore cardiac function. The topics included in the issue will cover the latest advances in dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), channelopathies, and derived complications of SARS-Cov2. Manuscript should pay special attention to key scientific discoveries, relevant to both basic and clinical research, emphasizing advances in molecular and structural biology, omics, stem cell research, electrophysiology, high-resolution imaging and disease modeling to understand the mechanistic nature of cardiac dysfunction in these conditions. The especial issue on “Cardiomyopathy: Pathogenesis, Diagnosis, and Treatment” seeks to provide a comprehensive understanding of the epidemiology, underlying mechanisms, natural course and recent therapeutic advances that can have an impact on the management and prognosis of patients with complex cardiomyopathies.

Dr. Juan A. Bernal
Guest Editor

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 submissions that pass pre-check are 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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

Keywords

  • dilated cardiomyopathy
  • arrhythmogenic cardiomyopathy
  • cardiac hypertrophy
  • SARS-CoV2 related injury
  • channelopathy
  • gene therapy
  • cardiomyocyte function
  • sarcomere pathophysiology

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Review

35 pages, 1494 KiB  
Review
The Microenvironment of the Pathogenesis of Cardiac Hypertrophy
by Farhad Bazgir, Julia Nau, Saeideh Nakhaei-Rad, Ehsan Amin, Matthew J. Wolf, Jeffry J. Saucerman, Kristina Lorenz and Mohammad Reza Ahmadian
Cells 2023, 12(13), 1780; https://doi.org/10.3390/cells12131780 - 4 Jul 2023
Cited by 7 | Viewed by 3075
Abstract
Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic [...] Read more.
Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic cardiomyopathy, is maladaptive. Here, we highlight the essential role and reciprocal interactions involving both cardiomyocytes and non-myocardial cells in response to pathological conditions. Prolonged cardiovascular stress causes cardiomyocytes and non-myocardial cells to enter an activated state releasing numerous pro-hypertrophic, pro-fibrotic, and pro-inflammatory mediators such as vasoactive hormones, growth factors, and cytokines, i.e., commencing signaling events that collectively cause cardiac hypertrophy. Fibrotic remodeling is mediated by cardiac fibroblasts as the central players, but also endothelial cells and resident and infiltrating immune cells enhance these processes. Many of these hypertrophic mediators are now being integrated into computational models that provide system-level insights and will help to translate our knowledge into new pharmacological targets. This perspective article summarizes the last decades’ advances in cardiac hypertrophy research and discusses the herein-involved complex myocardial microenvironment and signaling components. Full article
(This article belongs to the Special Issue Cardiomyopathy: Pathogenesis, Diagnosis, and Treatment)
Show Figures

Figure 1

Back to TopTop