Fibroblasts, myofibroblasts and cardiac arrhythmias.

J Cardiovasc Aging

The Wilf Family Cardiovascular Research Institute, Department of Medicine and Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

Published: October 2023


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10793996PMC
http://dx.doi.org/10.20517/jca.2023.37DOI Listing

Publication Analysis

Top Keywords

fibroblasts myofibroblasts
4
myofibroblasts cardiac
4
cardiac arrhythmias
4
fibroblasts
1
cardiac
1
arrhythmias
1

Similar Publications

[ alleviates bleomycin-induced pulmonary fibrosis in mice by inhibiting transformation of lung fibroblasts into myofibroblast].

Nan Fang Yi Ke Da Xue Xue Bao

August 2025

Key Laboratory of Tropical Biological Resources of Ministry of Education, School of Pharmaceutical Sciences, Hainan University, Haikou 570228, China.

Objectives: To investigate the effect of (HP) on bleomycin (BLM)-induced pulmonary fibrosis in mice and on TGF-β1-induced human fetal lung fibroblasts (HFL1).

Methods: Thirty male C57BL/6 mice were randomly divided into control group, BLM-induced pulmonary fibrosis model group, low- and high-dose HP treatment groups (3 and 21 mg/kg, respectively), and 300 mg/kg pirfenidone (positive control) group. The effects of drug treatment for 21 days were assessed by examining respiratory function, lung histopathology, and expression of fibrosis markers in the lung tissues of the mouse models.

View Article and Find Full Text PDF

Prim-O-glucosylcimifugin attenuates intestinal fibrosis by modulating TGF-β/MAPK signaling and ECM remodeling.

Life Sci

September 2025

KM Convergence Research Division, Korea Institute of Oriental Medicine, Republic of Korea; Korean Convergence Medical Science Major, KIOM School, University of Science & Technology (UST), Daejeon, 34054, Republic of Korea. Electronic address:

Background: Intestinal fibrosis is a severe and progressive complication of inflammatory bowel disease (IBD), particularly Crohn's disease (CD), for which no effective anti-fibrotic therapies currently exist.

Purpose: This study aimed to investigate the anti-fibrotic efficacy and underlying mechanisms of Prim-O-glucosylcimifugin (POG), a natural chromone derivative, in TGF-β1-stimulated human intestinal fibroblasts.

Methods: Fibrosis was modeled in human intestinal fibroblast cell lines (CCD-18Co) and human primary intestinal myofibroblasts (HIMF) using TGF-β1.

View Article and Find Full Text PDF

The tumor microenvironment (TME) of chronic inflammation-associated cancers (CIACs) is shaped by cycles of injury and maladaptive repair, yet the principles organizing fibrotic stroma in these tumors remain unclear. Here, we applied the concept of hot versus cold fibrosis, originally credentialed in non-cancerous fibrosis of heart and kidney, to lung squamous cell carcinoma (LUSC), a prototypical CIAC. Single-cell transcriptomics of matched tumor and adjacent-normal tissue from 16 treatment-naive LUSC patients identified a cold fibrotic architecture in the LUSC TME: cancer-associated fibroblasts (CAFs) expanded and adopted myofibroblast and stress-response states, while macrophages were depleted.

View Article and Find Full Text PDF

Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the formation of fluid filled cysts, progressive fibrosis and chronic inflammation, often leading to kidney failure. Renal fibrosis in ADPKD is primarily driven by myofibroblast activation and excessive extracellular matrix (ECM) accumulation, which contribute to disease progression. Here we investigated the therapeutic potential of pirfenidone, an antifibrotic drug, on myofibroblast activity, ECM production, and ADPKD progression.

View Article and Find Full Text PDF

Non-small cell lung cancer (NSCLC) is the most common lung cancer type and one of the deadliest neoplasias worldwide. NSCLC is histologically classified into adenocarcinoma, squamous cell carcinoma, and other less frequent subtypes. Both subtypes and other solid tumors are increasingly regarded as abnormal organs, highlighting the critical role of the desmoplastic tumor stroma rich in cancer-associated fibroblasts (CAFs) in driving tumor progression and therapeutic resistance.

View Article and Find Full Text PDF