The endothelium, an essential component of the vascular system, plays a critical role in the inflammatory response. Under pro-inflammatory stimuli, endothelial cells undergo activation and dysfunction, leading to the release of inflammatory mediators and upregulation of cell adhesion molecules. These changes facilitate the adhesion, rolling, and transmigration of leukocytes into the subendothelial space. Emerging evidence suggests that epigenetic mechanisms, including nucleic acid methylation, post-translational histone modifications, and non-coding RNA, contribute significantly to the regulation of vascular inflammation and expression of cell adhesion molecules. Understanding the epigenetic molecular signatures that govern these processes may provide new insights into the development of therapeutic strategies to combat vascular inflammation and associated diseases. This review aims to summarize the current knowledge on the epigenetic mechanisms involved in modulating the intricate processes underlying vascular inflammation, with a specific focus on the expression of endothelial adhesion molecules and endothelium-leukocyte adhesion.
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http://dx.doi.org/10.31083/j.fbl2809194 | DOI Listing |
Cardiovasc Diabetol
January 2025
Facultat de Medicina i Ciències de la Salut, Unitat de Recerca en Lípids i Arteriosclerosi, Universitat Rovira i Virgili, Reus, Spain.
Backgrounds And Aims: Preclinical studies suggest that a triglyceride (TG)-independent proinflammatory action of apolipoprotein C-III (apoCIII) exists. We aimed to investigate the relationship between circulating apoCIII levels and subclinical inflammation markers across different cohorts with distinctive inflammatory patterns: patients with metabolic disorders (MDs), patients with rheumatoid arthritis (RA), and controls. Specifically, we assessed the associations of apoCIII with acute inflammation biomarkers (e.
View Article and Find Full Text PDFNat Cardiovasc Res
January 2025
Department of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Atherosclerotic lesions develop preferentially in arterial regions exposed to disturbed blood flow, where endothelial cells acquire an inflammatory phenotype. How disturbed flow induces endothelial cell inflammation is incompletely understood. Here we show that histone H3.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Spinal Surgery, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Inflammation aggravates secondary damage following spinal cord injury (SCI). M1 microglia induce inflammation and exert neurotoxic effects, whereas M2 microglia exert anti-inflammatory and neuroprotective effects. The sine oculis homeobox (SIX) gene family consists of six members, including sine oculis homeobox homolog 1 (SIX1)-SIX6.
View Article and Find Full Text PDFDig Dis Sci
January 2025
Department of Gastroenterology and Hepatology, Amsterdam University Medical Centres, Location AMC, Meibergdreef 9, 1105AZ, Amsterdam, The Netherlands.
Aims: Duodenal Mucosal Resurfacing (DMR) is an endoscopic ablation technique aimed at improving glycemia in patients with type 2 diabetes mellitus (T2DM). Although the exact underlying mechanism is still unclear, it is postulated that the DMR-induced improvements are the result of changes in the duodenal mucosa. For this reason, we assessed macroscopic and microscopic changes in the duodenal mucosa induced by DMR + GLP-1RA.
View Article and Find Full Text PDFCurr Drug Targets
January 2025
Department of Pharmacology, SVKM's Institute of Pharmacy, Dhule, 424001, India.
Currently, diabetic nephropathy (DN) stands as the predominant global cause of endstage renal disease. Many scientists believe that diabetes will eventually spread to pandemic levels due to the rising prevalence of the disease. While the primary factor leading to diabetic nephropathy is vascular dysfunction induced by hyperglycemia, several other pathological elements, such as fibrosis, inflammation, and oxidative stress, also contribute to the progression of the disease.
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