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Role of TGFbeta Ligand Function in the Development and Pathogenesis...
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Role of TGFbeta Ligand Function in the Development and Pathogenesis of Cardiovascular Disease

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Basic and Translational Cardiovascular Research".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 2261

Special Issue Editors

Dr. Mohamad Azhar

E-Mail Website
Guest Editor
Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29209, USA
Interests: transforming growth factor; cardiovascular development; valve development; valvular heart disease; aortic aneurysm; aortic calcification
Dr. Chetan Hans

E-Mail Website
Guest Editor
Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
Interests: abdominal aortic aneurysm
Dr. Nimrat Grewal

E-Mail Website
Guest Editor
Cardiothoracic Surgery, Leiden University Medical Center, Leiden, The Netherlands
Interests: aortic valve; heart valve diseases; vascular surgery; aneurysm cardiac surgery; aortic diseases; atherosclerotic vascular diseases; cardiovascular surgery; coronary artery bypass surgery; endovascular surgery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We welcome review and original article contributions that increase our understanding of the transforming growth factor beta (TGFB) pathway in cardiovascular development and disease. TGFB ligands (TGFB1,2,3) are multifunctional growth factors and cytokines that are produced in latent form by most cardiac cell types during cardiovascular development and in adult cardiovascular tissues. All TGFB ligands bind to the TGFBR1 and TGFBR2 receptor complex. Downstream signaling occurs through phosphorylation and nuclear translocation of SMAD2 and SMAD3 in conjunction with SMAD4. In addition, the TGFB ligand–receptor complex also activates non-canonical pathways involving the MAP kinase pathway (TAK, p38, ERK1/2 MAPK). TGFB-regulated gene expression controls cell differentiation, cell growth, apoptosis, cell migration, and extracellular matrix production and remodeling during cardiovascular development and pathogenesis of cardiovascular disease. Genetic mutations in TGFB2 and TGFB3 cause congenital heart disease, bicuspid aortic valve, mitral valve disease, and aortic aneurysm and dissection in patients of Loeys–Dietz syndrome. Increased TGFB1 expression is associated with cardiomyopathy, mitral valve prolapse, and aortic aneurysm in Marfan syndrome. Increased TGFB signaling is found in cardiac fibrosis, cardiac hypertrophy, myocardial infarction and heart failure, hypertension, atherosclerosis, arterial calcification, and thoracic and abdominal aortic aneurysms. Thus, understanding the cell-specific role and molecular and biochemical mechanisms of TGFβ ligands will lead to safer and more effective therapy for cardiovascular disease. Consequently, we invite author contributions that advance our current understanding of TGFβ signaling in cardiovascular development and cardiovascular disease. We suggest the following themes for this Special Issue:

  • TGFβ in cardiovascular development;
  • TGFβ in aortopathy: thoracic and abdominal aneurysm, arterial calcification, atherosclerosis;
  • TGFβ in bicuspid aortic valve, mitral valve disease, aortic valve calcification, aortic stenosis;
  • TGFβ in cardiac hypertrophy, cardiac fibrosis, heart failure;
  • TGFβ in hypertension and atherosclerosis;
  • TGFβ signaling mechanism using in vitro cell and tissue culture models;
  • Novel models of TGFβ signaling in the cardiovascular system;

TGFβ-based therapies of cardiovascular disease and cardiotoxicity.

Dr. Mohamad Azhar
Dr. Chetan Hans
Dr. Nimrat Grewal
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 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. Journal of Cardiovascular Development and Disease is an international peer-reviewed open access monthly 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

  • transforming growth factor beta
  • TGFB1
  • TGFB2
  • TGFB3
  • aortic valve
  • aneurysm
  • mitral valve
  • congenital heart disease
  • fibrosis
  • hypertrophy
  • hypertension
  • atherosclerosis
  • peripheral artery disease
  • heart failure

Published Papers (1 paper)

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Research

14 pages, 3943 KiB  
Article
Activation of AcvR1-Mediated Signaling Results in Semilunar Valve Defects
by Shabber Syed, Sudha Rajderkar, Jeffrey M. Mann, Travis Hawkins, Bingrou Wu, Bin Zhou, Yukiko Sugi, Yuji Mishina and Vesa Kaartinen
J. Cardiovasc. Dev. Dis. 2022, 9(8), 272; https://doi.org/10.3390/jcdd9080272 - 16 Aug 2022
Viewed by 1931
Abstract
Calcific aortic valve disease (CAVD) is a common cardiac defect, particularly in the aging population. While several risk factors, such as bi-leaflet valve structure and old age, have been identified in CAVD pathogenesis, molecular mechanisms resulting in this condition are still under active [...] Read more.
Calcific aortic valve disease (CAVD) is a common cardiac defect, particularly in the aging population. While several risk factors, such as bi-leaflet valve structure and old age, have been identified in CAVD pathogenesis, molecular mechanisms resulting in this condition are still under active investigation. Bone morphogenetic protein signaling via the activin type I receptor (AcvRI) plays an important role during physiological and pathological processes involving calcification, e.g., bone formation and heterotopic ossification. In addition, AcvRI is required for normal cardiac valve development, yet its role in aortic valve disease, if any, is currently unknown. Here, we induced the expression of constitutively active AcvRI in developing mouse embryos in the endocardium and in cells at the valve leaflet–wall junction that are not of endocardium origin using the Nfac1Cre transgene. The mutant mice were born alive, but showed thickened aortic and pulmonary valve leaflets during the early postnatal period. Adult mutant mice developed aortic stenosis with high frequency, sclerotic aortic valves, and displayed Alcian Blue-positive hypertrophic chondrocyte-like cells at the leaflet–wall junction. Calcification was only seen with low penetrance. In addition, we observed that the expression levels of gene sets associated with inflammation-related cytokine signaling, smooth muscle cell contraction, and cGMP signaling were altered in the mutants when compared with those of the controls. This work shows that, in a mouse model, such continuous AcvRI activity in the Nfatc1Cre recombination domain results in pathological changes in the aortic valve structure and function. Full article
(This article belongs to the Special Issue Role of TGFbeta Ligand Function in the Development and Pathogenesis of Cardiovascular Disease)
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