The complex syndrome of heart failure (HF) is characterized by increased left ventricular pressures. Cardiomyocytes increase in size, cardiac fibroblasts transform and make extracellular matrix, and leukocytes infiltrate the cardiac tissue and alter cardiomyocyte and cardiac fibroblast function. Here we review recent advances in our understanding of the cellular composition of the heart during homeostasis and in response to cardiac pressure overload, with an emphasis on immune cell communication with cardiac fibroblasts and its consequences in cardiac remodeling.
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http://dx.doi.org/10.1016/j.cophys.2022.100484 | DOI Listing |
Front Cardiovasc Med
January 2025
Department of Cardiology, Liuzhou Workers' Hospital, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, China.
Background: Fibroblasts in the fibrotic heart exhibit a heterogeneous biological behavior. The specific subsets of fibroblasts that contribute to progressive cardiac fibrosis remain unrevealed. Our aim is to identify the heart fibroblast (FB) subsets that most significantly promote fibrosis and the related critical genes as biomarkers for ischemic heart disease.
View Article and Find Full Text PDFHeliyon
January 2025
Department of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
The extracellular matrix (ECM) is a complex and dynamic three-dimensional network that functions as an architectural scaffold to maintain cardiac homeostasis. Important biochemical and mechanical signals associated with cell‒cell communication are provided via the reciprocal interaction between cells and the ECM. By converting mechanical cues into biochemical signals, the ECM regulates many cell processes, including migration, adhesion, growth, differentiation, proliferation, and apoptosis.
View Article and Find Full Text PDFJ Mol Cell Cardiol
January 2025
Department of Cardiology, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250031, PR China. Electronic address:
Background: Takotsubo syndrome (TTS) primarily manifests as a cardiomyopathy induced by physical or emotional stress, remains a poorly understood condition with no established treatments. In this study, we investigated the potential of sacubitril/valsartan (sac/val) to increase the survival of TTS patients and reduce inflammation and myocardial fibrosis in experimental models.
Aim: This study aimed to evaluate whether sac/val could improve survival rates in TTS patients, mitigate cardiac remodeling in vivo, and explore its anti-inflammatory and antifibrotic mechanisms in vitro.
Eur Heart J
January 2025
School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, 2199 Lishui Rd, Nanshan, Shenzhen, Guangdong Province 518055, China.
Background And Aims: Lackluster results from recently completed gene therapy clinical trials of VEGF-A delivered by viral vectors have heightened the need to develop alternative delivery strategies. This study aims to demonstrate the pre-clinical efficacy and safety of extracellular vesicles (EVs) loaded with VEGF-A mRNA for the treatment of ischaemic vascular disease.
Methods: After encapsulation of full-length VEGF-A mRNA into fibroblast-derived EVs via cellular nanoporation (CNP), collected VEGF-A EVs were delivered into mouse models of ischaemic injury.
Int J Nanomedicine
January 2025
Department of Emergency and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, People's Republic of China.
Purpose: Cardiac fibrosis, a key contributor to ventricular pathologic remodeling and heart failure, currently lacks effective therapeutic approaches.
Patients And Methods: Small extracellular vesicles from young healthy human plasma (Young-sEVs) were characterized via protein marker, transmission electron microscopy, and nanoparticle tracking analysis, then applied in cellular models and mouse models of cardiac fibrosis. Western blotting and qRT-PCR were used to identify protective signaling pathways in cardiac fibroblasts (CFs).
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