Cardiovascular Diseases: From Bench to Bedside

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 1054

Special Issue Editor


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Guest Editor
1. Department of Medicine and Health Sciences “Vincenzo Tiberio”, University of Molise, Campobasso, Italy
2. Departments of Medicine and Molecular Pharmacology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, New York, NY, USA
Interests: hypertension; diabetes; heart failure; coronary artery disease; frailty; cognitive impairment

Special Issue Information

Dear Colleagues,

Cardiovascular diseases increase the risk of hospitalization, death, and adverse events, particularly in older adults. Indeed, cardiovascular diseases drive the risk of frailty with functional impairment. In this scenario, a prompt diagnosis and careful prevention are key to reduce/delay the aforementioned complications. Hereafter, we want to stress the importance of managing cardiovascular diseases to prevent adverse outcomes. The aim of our Special Issue is to summarize the mechanisms underlying the progression of the main cardiovascular diseases (such as heart failure, hypertension, coronary artery disease etc.), focusing on complications. Hence, both clinical and pre-clinical manuscripts are welcome.

Dr. Pasquale Mone
Guest Editor

Manuscript Submission Information

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Keywords

  • hypertension
  • heart failure
  • coronary artery disease
  • ischemia with no obstructive coronary artery disease
  • acute myocardial infarction
  • cardiovascular diseases in frail individuals
  • cardiovascular diseases in older adults

Published Papers (1 paper)

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Research

21 pages, 6749 KiB  
Article
The Role of Matrix Metalloproteinases in Thoracic Aortic Disease: Are They Indicators for the Pathogenesis of Dissections?
by Marc Irqsusi, Lan Anh Dong, Fiona R. Rodepeter, Rabia Ramzan, Ildar Talipov, Tamer Ghazy, Madeline Günther, Sebastian Vogt and Ardawan J. Rastan
Biomedicines 2024, 12(3), 619; https://doi.org/10.3390/biomedicines12030619 - 9 Mar 2024
Viewed by 863
Abstract
The pathogenesis of aortic aneurysm and dissection continues to be under discussion. Extracellular matrix (ECM) remodeling processes in the aortic wall are hypothesized to be involved in the development of the disorders. Therefore, in a histological study, we investigated the expression of metalloproteases [...] Read more.
The pathogenesis of aortic aneurysm and dissection continues to be under discussion. Extracellular matrix (ECM) remodeling processes in the aortic wall are hypothesized to be involved in the development of the disorders. Therefore, in a histological study, we investigated the expression of metalloproteases 1 and 9 (MMP1 and MMP9) and their inhibitors (TIMP 1 and TIMP 2) in cardiac surgery patients. In parallel, we studied the aortic roots by echocardiography. Clinical reports of 111 patients (30 women and 81 men) who suffered from aortic aneurysms and aortic dissection were evaluated and studied by transesophageal echocardiography. Seven patients who had coronary heart disease served as “healthy controls”. All patients underwent the necessary surgical procedure according to the diagnosed aortic disease in the period from 2007 to 2015. A tissue sample of the aortic biopsies was collected from each patient during surgery. Immunohistochemical staining was performed for MMP1 and MMP9 and TIMP1 and TIMP2 as well. Vascularization was monitored by a CD 31 antibody. In direct comparison, the expressions are not homogeneous. We found the smallest changes in the intima area at all. TIMP 1 and TIMP 2 distribution increases from the lumen of the vessel outward in the wall layers of the aorta. In the case of arteriosclerotic changes, intima had a capillarization, but not in the media. An opposite pattern was found in the dissected aortas. There are differences in the vascularization between the aneurysm and dissection and the different layers, respectively. A different remodeling process of the ECM in comparison to the vascular layers must be hypothesized. Reading the patterns of staining and with regard to the known inhibitory effect of MMP9 on ECM remodeling, but especially TIMP 2 on neoangiogenesis, disturbed nutrition, and dysfunctional vasa vasorum remodeling must be assumed as causes of dissection. Full article
(This article belongs to the Special Issue Cardiovascular Diseases: From Bench to Bedside)
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