miRNA Regulation of Cell Phenotype and Parietal Remodeling in Atherosclerotic and Non-Atherosclerotic Aortic Aneurysms: Differences and Similarities.

Marfan syndrome abdominal aortic aneurysm atherosclerosis bicuspid aortic valve calcification endothelial dysfunction fibrosis miRNA deregulation smooth muscle cell dedifferentiation thoracic aortic aneurysm

Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
24 Feb 2024
Historique:
received: 02 02 2024
revised: 21 02 2024
accepted: 22 02 2024
medline: 13 3 2024
pubmed: 13 3 2024
entrez: 13 3 2024
Statut: epublish

Résumé

Aortic aneurysms are a serious health concern as their rupture leads to high morbidity and mortality. Abdominal aortic aneurysms (AAAs) and thoracic aortic aneurysms (TAAs) exhibit differences and similarities in their pathophysiological and pathogenetic features. AAA is a multifactorial disease, mainly associated with atherosclerosis, characterized by a relevant inflammatory response and calcification. TAA is rarely associated with atherosclerosis and in some cases is associated with genetic mutations such as Marfan syndrome (MFS) and bicuspid aortic valve (BAV). MFS-related and non-genetic or sporadic TAA share aortic degeneration with endothelial-to-mesenchymal transition (End-Mt) and fibrosis, whereas in BAV TAA, aortic degeneration with calcification prevails. microRNA (miRNAs) contribute to the regulation of aneurysmatic aortic remodeling. miRNAs are a class of non-coding RNAs, which post-transcriptionally regulate gene expression. In this review, we report the involvement of deregulated miRNAs in the different aortic remodeling characterizing AAAs and TAAs. In AAA, miRNA deregulation appears to be involved in parietal inflammatory response, smooth muscle cell (SMC) apoptosis and aortic wall calcification. In sporadic and MFS-related TAA, miRNA deregulation promotes End-Mt, SMC myofibroblastic phenotypic switching and fibrosis with glycosaminoglycan accumulation. In BAV TAA, miRNA deregulation sustains aortic calcification. Those differences may support the development of more personalized therapeutic approaches.

Identifiants

pubmed: 38473887
pii: ijms25052641
doi: 10.3390/ijms25052641
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : European Union-Next Generation UE
ID : PNRR-MR1-2022-12376699

Auteurs

Sonia Terriaca (S)

Anatomic Pathology, Policlinico Tor Vergata, 00133 Rome, Italy.

Amedeo Ferlosio (A)

Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University, 00133 Rome, Italy.

Maria Giovanna Scioli (MG)

Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University, 00133 Rome, Italy.

Francesca Coppa (F)

Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University, 00133 Rome, Italy.

Fabio Bertoldo (F)

Cardiac Surgery Unit, Department of Surgery, Tor Vergata University, 00133 Rome, Italy.

Calogera Pisano (C)

Cardiac Surgery Unit, Department of Surgery, Tor Vergata University, 00133 Rome, Italy.

Beatrice Belmonte (B)

Tumor Immunology Unit, Department of Health Sciences, University of Palermo, 90134 Palermo, Italy.
Azienda sanitaria Provinciale di Catania (ASP), 95124 Catania, Italy.

Carmela Rita Balistreri (CR)

Cellular and Molecular Laboratory, Department of Biomedicine, Neuroscience and Advanced Diagnostics (Bi.N.D.), University of Palermo, 90134 Palermo, Italy.

Augusto Orlandi (A)

Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University, 00133 Rome, Italy.

Classifications MeSH