American Journal Of Pathology, Journal Year: 2025, Volume and Issue: unknown
Published: June 1, 2025
Language: Английский
Nature Reviews Cardiology, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 13, 2025
Language: Английский
Citations
3
Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
The modification of endothelial cells (ECs) biological function under pathogenic conditions leads to the expression mesenchymal stromal (MSCs) markers, defined as endothelial-to-mesenchymal transition (EndMT). Invisible in onset and slow progression, atherosclerosis (AS) is a potential contributor various atherosclerotic cardiovascular diseases (ASCVD). By triggering AS, EndMT, "initiator" induces progression ASCVD such coronary heart disease (CHD) ischemic cerebrovascular (ICD), with serious clinical complications myocardial infarction (MI) stroke. In-depth research pathomechanisms EndMT identification targeted therapeutic strategies hold considerable value for prevention treatment ASCVD-associated delayed EndMT. Although previous studies have progressively unraveled complexity its pathogenicity triggered by alterations vascular microenvironmental factors, systematic descriptions most recent roles strategies, their future directions are scarce.
Language: Английский
Citations
2
Trends in Endocrinology and Metabolism, Journal Year: 2024, Volume and Issue: unknown
Published: Dec. 1, 2024
Endothelial cells (ECs) form the inner lining of blood vessels that is crucial for vascular function and homeostasis. They regulate tone, oxidative stress, permeability. Dysfunction leads to increased permeability, leukocyte adhesion, thrombosis. ECs undergo metabolic changes in conditions such as wound healing, cancer, atherosclerosis, diabetes, can influence disease progression. We discuss recent research has revealed diverse intracellular pathways are tailored their functional needs, including lipid handling, glycolysis, fatty acid oxidation (FAO). Understanding EC signatures health will be not only basic biology but also exploited when designing new therapies target EC-related functions different diseases.
Language: Английский
Citations
7
BMC Cardiovascular Disorders, Journal Year: 2025, Volume and Issue: 25(1)
Published: Feb. 17, 2025
This study aimed to identify novel candidates that regulate Endothelial mesenchymal transition(EndMT) in atherosclerosis by integrating multi-omics data. The single-cell RNA sequencing (scRNA-seq) dataset GSE159677, bulk RNA-seq GSE118446 and microarray GSE56309 were obtained from the Gene Expression Omnibus (GEO) database. uniform manifold approximation projection (UMAP) used for downscaling cluster identification. Differentially expressed genes (DEGs) analyzed using limma package. Functional enrichment analysis was applied DAVID functional annotation tool. Quantitative real-time polymerase chain reaction (qPCR) western blotting further validation. Nine endothelial cell (EC) clusters identified human plaques, with EC 5 exhibiting an EndMT phenotype. intersection of common DEGs vitro models revealed seven candidates: PTGS2, TPM1, SERPINE1, FN1, RASD1, SEMA3C, ESM1. Validation these findings carried out through qPCR analysis. Through integration data bioinformatics methods, our
Language: Английский
Citations
1
Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)
Published: Feb. 19, 2025
Angiogenesis and osteogenesis are closely interrelated. The interaction between endothelial bone-forming cells, such as osteoblasts, is crucial for normal bone development repair. Juxtacrine paracrine mechanisms play key roles in cell differentiation towards the osteogenic direction, assuming direct effect of endothelium on differentiation. However, this interplay have yet to be thoroughly studied. Isolated cells (EC) from human umbilical vein osteoblasts (OB) epiphysis femur or tibia were cultured indirect (separated by membrane) contact vitro under conditions. Osteogenic was verified RT-PCR, alizarin red staining. Shotgun proteomics RNA-sequencing used compare both EC OB different co-culture conditions assess EC-OB interplay. To verify role Notch signaling, experiments with modulation performed lentiviral transduction further co-cultivation OB. Additionally, assessed RNA-sequencing. opposite effects depending In contact, enhance differentiation, but cultures, suppress it. Our proteotranscriptomic analysis revealed that osteosuppressive related action factors secreted EC, while osteoinductive properties mediated signaling pathway, which can activated only upon a physical Indeed, co-culture, knockdown Notch1 Notch3 receptors has an inhibitory whereas activation intracellular domain either inductive data indicate dual regulating highlight unique pathway inducing during cell-to-cell interactions. findings study emphasize importance intercellular communication regulation osteoblast maintenance.
Language: Английский
Citations
1
International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(5), P. 2139 - 2139
Published: Feb. 27, 2025
Dengue virus (DV) infection poses a severe life-threatening risk in certain cases. This is mainly due to endothelial dysregulation, which causes plasma leakage and hemorrhage. However, the etiology of DV-induced dysregulation remains incompletely understood. To identify potential mechanisms caused by DV, effects conditioned media from (CMDV) on mechanics transcriptional profile cells were examined using permeability assays, atomic force microscopy, In-Cell Western blot silico transcriptomics. Exposure HMEC-1 CMDV increased cellular stiffness. It also induced expression key proteins associated with endothelial-to-mesenchymal transition (EndMT). These data support notion that DV promotes dysfunction triggering programs compromise barrier function. Understanding molecular underlying crucial for developing targeted therapeutic strategies mitigate outcomes dengue infection.
Language: Английский
Citations
1
Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16
Published: March 17, 2025
Cardiac immune-related adverse events (irAEs) from PD-1-targeting immune check-point inhibitors (ICIs) are an increasing concern due to their high mortality rate. Collagen plays a crucial role in maintaining cardiac structure, elasticity, and signal transduction; however, the effects mechanisms of PD-1 inhibitor on collagen remodeling remain poorly understood. C57BL/6 mice were injected with anti-mouse antibody create inhibitor-treated model. function was measured by echocardiography, distribution analyzed Masson's trichrome staining Sirius Red staining. Single-nucleus RNA sequencing performed examine inhibition gene expression fibroblasts (CFs) endothelial cells (ECs). EC-CF crosstalk assessed using co-culture experiments ELISA. ChIP assay analyze regulation TCF12 TGF-β1 promoter. Western blot, qRT-PCR, immunofluorescence used detect TCF12, TGF-β1, endothelial-to-mesenchymal transition (EndMT) markers. Reactive oxygen species (ROS) levels evaluated DHE staining, MDA content, SOD activity assays. We report newly discovered cardiotoxic effect inhibitor, which causes aberrant heart, marked decrease interstitial increase perivascular deposition. Mechanistically, does not directly affect CFs but instead impact them through crosstalk. reduces secretion ECs downregulating we identify as transcriptional promoter TGF-β1. This subsequently decreases CF activity, leading reduced Additionally, induces EndMT, The dysfunction induced results ROS accumulation ECs. Inhibiting N-acetylcysteine (NAC) preserves normal reversing downregulation EndMT Our suggest that ECs, imbalanced (decrease collagen) heart modulating TCF12/TGF-β1-mediated EndMT. NAC supplementation could be effective clinical strategy mitigate inhibitor-induced dysfunction.
Language: Английский
Citations
1
Circulation Research, Journal Year: 2025, Volume and Issue: 136(11), P. 1433 - 1453
Published: May 22, 2025
Cardiovascular diseases including atherosclerosis and heart failure, arise from the intricate interplay of metabolic, immune, neural dysregulation within vascular cardiac tissues: This review focuses on integrating recent advances in metabolic immune crosstalk vasculature that affects cardiometabolic health disease progression. Coronary lymphatic endothelial cells regulate metabolism, their dysfunction is linked to cardiovascular diseases. Lymphatics maintain tissue homeostasis, clearing waste, lipids, cells, maladaptation worsens outcomes. Altered metabolism failure drives immune-mediated inflammation, fibrosis, adverse remodeling. Concurrently, artery tertiary lymphoid organs formed adventitia advanced atherosclerotic arteries, serve as pivotal neuroimmune hubs, coordinating local immunity through T B cell activation neurovascular signaling via artery-brain circuits. plaques undergo clonal expansion a result peripheral tolerance breakdown, with proinflammatory CD4 + CD8 subsets amplifying atherosclerosis, effects further shaped by systemic activation. Therapeutic strategies targeting dysfunction, crosstalk, plasticity hold promise for integrated management.
Language: Английский
Citations
1
Circulation Research, Journal Year: 2025, Volume and Issue: 136(11), P. 1262 - 1285
Published: May 22, 2025
Heart failure (HF) often coexists with cancer. Beyond the known cardiotoxicity of some cancer treatments, HF itself has been associated increased incidence. The 2 conditions share common risk factors, mechanisms, and interactions that can worsen patient outcomes. bidirectional relationship between presents a complex interplay factors are not fully understood. Recent preclinical evidence suggests may promote tumor growth via release protumorigenic from injured heart, revealing as potentially condition. Our review discusses biological crosstalk cancer, emphasizing impact on growth, inflammation, modulating immune system central mechanisms. We further explore clinical implications this connection propose future research directions. Understanding mechanistic overlap could lead to new biomarkers therapies, addressing growing prevalence both enhancing approaches diagnosis, prevention, treatment.
Language: Английский
Citations
1
Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 174, P. 116589 - 116589
Published: April 17, 2024
Diabetic cardiomyopathy (DCM) is a common severe complication of diabetes that occurs independently hypertension, coronary artery disease, and valvular cardiomyopathy, eventually leading to heart failure. Previous studies have reported Tectorigenin (TEC) possesses extensive anti-inflammatory anti-oxidative stress properties. In this present study, the impact TEC on diabetic was examined. The model DCM in mice established with combination high-fat diet STZ treatment. Remarkably, treatment significantly attenuated cardiac fibrosis improved dysfunction. Concurrently, also found mitigate hyperglycemia hyperlipidemia mouse. At molecular level, involved activation AMPK, both vitro vivo, by enhancing its phosphorylation. This achieved through regulation endothelial-mesenchymal transition via AMPK/TGFβ/Smad3 pathway. Furthermore, it demonstrated level ubiquitination adiponectin receptor 1 (AdipoR1) protein associated TEC-mediated improvement dysfunction mice. Notably substantial reduction myocardial fibrosis. conclusion, improves modulating AdipoR1/AMPK signaling These findings suggest could be an effective therapeutic agent for cardiomyopathy.
Language: Английский
Citations
5