AI Article Synopsis
- Syndecan-4 is a type of proteoglycan that plays a role as a transmembrane receptor and is part of a four-member family.
- Genetic removal of Syndecan-4 in mice doesn't cause major developmental issues, but it leads to noticeable differences under stress or challenges.
- The review focuses on how Syndecan-4 is involved in heart cell functions, especially during injury and the healing process.
Article Abstract
The heparan sulphate proteoglycan Syndecan-4 belongs to a 4-member family of transmembrane receptors. Genetic deletion of Syndecan-4 in mice causes negligible developmental abnormalities however when challenged these animals show distinct phenotypes. Synedcan-4 is expressed in many cell types in the heart and its expression is elevated in response to cardiac injury and recent studies have suggested roles for Syndecan-4 in repair mechanisms within the damaged heart. The purpose of this review is to explore these biological insights into the role of Syndecan-4 in both the injured heart and later during cardiac repair and remodeling.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.biocel.2022.106196 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
PTN secreted by cardiac fibroblasts promotes myocardial fibrosis and inflammation of pressure overload-induced hypertrophic cardiomyopathy through the PTN-SDC4 pathway.
Life Sci
January 2025
Basic Medical Research Center, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. Electronic address:
Aims: Hypertrophic cardiomyopathy (HCM) is characterized by unexplained left ventricular hypertrophy (LVH) with key pathologic processes including myocardial necrosis, fibrosis, inflammation, and hypertrophy, which are involved in heart failure (HF), stroke, and even sudden death. Our aim was to explore the communication network among various cells in the heart of transverse aortic constriction (TAC) surgery induced HCM mice.
Materials And Methods: Single-cell RNA-seq data of GSE137167 was downloaded from the Gene Expression Omnibus (GEO) database.
Wooden breast myopathy is characterized by satellite cell dysfunction and syndecan-4 shedding.
Front Physiol
December 2024
Raw Materials and Optimalization, Nofima AS, Ås, Norway.
Introduction: Skeletal muscle satellite cells (MuSCs or stem cells) play a crucial role in muscle development, maintenance, and regeneration, supporting both hypertrophy and regenerative myogenesis. Syndecans (SDCs) act as communication bridges within the muscle microenvironment, regulating interactions with extracellular matrix components and contributing significantly to tissue repair and inflammation. Specifically, syndecan-4 (SDC4) is involved in muscle regeneration at multiple stages.
View Article and Find Full Text PDFFBLN7 mediates vascular smooth muscle cell phenotype switching and vascular remodeling in hypertension.
Theranostics
December 2024
State Key Laboratory for Innovation and Transformation of Luobing Theory; Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Arterial remodeling serves as a pivotal mechanism underlying the development of diseases such as hypertension. Fibulin-7 (FBLN7), an adhesion protein, remains enigmatic regarding its role in these pathological processes. This study aims to explore whether FBLN7 influences vascular remodeling and its underlying mechanisms.
View Article and Find Full Text PDFEndothelial eNOS deficiency causes podocyte injury through NFAT2 and heparanase in diabetic mice.
Sci Rep
November 2024
Division of Nephrology and Hypertension, Vanderbilt University Medical Center, S-3223, MCN, Nashville, TN, 37232, USA.
The pivotal role of endothelial nitric oxide synthase (eNOS) in diabetic nephropathy (DN) has been demonstrated using global eNOS knockout (eNOSGKO) mice. However, the precise role of endothelially expressed eNOS and how its deficiency advances DN are still unclear. Here, we targeted endothelial eNOS expression (E-eNOSKO) after the onset of diabetes using the floxed eNOS and endSCL-CreER alleles.
View Article and Find Full Text PDFSDC4 protein action and related key genes in nonhealing diabetic foot ulcers based on bioinformatics analysis and machine learning.
Int J Biol Macromol
December 2024
Department of Burns and Plastic Surgery, Beijing Jishuitan Hospital, Capital Medical University, Beijing 100035, China. Electronic address:
Diabetic foot ulcers (DFU) is a complication associated with diabetes characterised by high morbidity, disability, and mortality, involving chronic inflammation and infiltration of multiple immune cells. We aimed to identify the critical genes in nonhealing DFU using single-cell RNA sequencing, transcriptomic analysis and machine learning. The GSE165816, GSE134431, and GSE143735 datasets were downloaded from the GEO database.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!