Excessive inflammatory signaling and pathological remodeling of the extracellular matrix drive cardiac fibrosis and require changes in gene expression. Using bioinformatics, both tissue-specific expression profiles and epigenomic profiles of some genes critical for cardiac fibrosis were examined, namely, (encodes angiotensin II precursors) and (post-transcriptionally regulates ). In monocytes, neutrophils, fibroblasts, venous cells, liver and brain, enhancers or super-enhancers were found that correlate with high expression of these genes. One enhancer extended into a silent gene neighbor. These enhancers harbored tissue-specific foci of DNA hypomethylation, open chromatin and transcription factor binding. This study identified previously undescribed enhancers containing hypomethylated transcription factor binding subregions that are predicted to regulate expression of these cardiac fibrosis-inducing genes.
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http://dx.doi.org/10.2217/epi-2020-0446 | DOI Listing |
Mol Cell Biochem
January 2025
Department of Cardiology, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory, Disease, Guangzhou Institute of Cardiovascular Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, Guangdong, China.
Increased activity of acid sphingomyelinase (ASMase) has been linked to diabetes and organ fibrosis. Nevertheless, the precise influence of ASMase on diabetic myocardial fibrosis and the corresponding molecular mechanisms remain elusive. In this study, we aim to elucidate whether ASMase contributes to diabetic myocardial fibrosis through the phosphorylation mediated by MAPK, thereby culminating in the development of diabetic cardiomyopathy (DCM).
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Pharmacology, Central University of Punjab, Bathinda, Punjab, 151401, India.
Diabetic cardiomyopathy (DCM) represents a significant health burden, exacerbated by the global increase in type 2 diabetes mellitus (T2DM). This condition contributes substantially to the morbidity and mortality associated with diabetes, primarily through myocardial dysfunction independent of coronary artery disease. Current treatment strategies focus on managing symptoms rather than targeting the underlying pathophysiological mechanisms, highlighting a critical need for specific therapeutic interventions.
View Article and Find Full Text PDFColomb Med (Cali)
January 2025
Karabuk University Faculty of Medicine, Department of Cardiology, Karabuk, Turkey Karabük University Karabuk University Faculty of Medicine Department of Cardiology Karabuk Turkey.
Background: The association of fragmented QRS (fQRS) with many cardiac pathologies such as cardiac fibrosis has been described previously. Paraaortic adipose tissue (PAT) is thought to be associated with many cardiac diseases and there is only one publication on its echocardiographic evaluation.
Aims: To describe the possible relationship between fQRS and PAT.
Front Immunol
January 2025
Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao, China.
CCL2, a pivotal cytokine within the chemokine family, functions by binding to its receptor CCR2. The CCL2/CCR2 signaling pathway plays a crucial role in the development of fibrosis across multiple organ systems by modulating the recruitment and activation of immune cells, which in turn influences the progression of fibrotic diseases in the liver, intestines, pancreas, heart, lungs, kidneys, and other organs. This paper introduces the biological functions of CCL2 and CCR2, highlighting their similarities and differences concerning fibrotic disorders in various organ systems, and reviews recent progress in the diagnosis and treatment of clinical fibrotic diseases linked to the CCL2/CCR2 signaling pathway.
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