Roles and Potential Mechanisms of Endothelial Cell-Derived Extracellular Vesicles in Ischemic Stroke

Translational Stroke Research, Год журнала: 2025, Номер unknown

Опубликована: Фев. 7, 2025

Язык: Английский

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Endothelial Dysfunction: Redox Imbalance, NLRP3 Inflammasome, and Inflammatory Responses in Cardiovascular Diseases

Antioxidants, Год журнала: 2025, Номер 14(3), С. 256 - 256

Опубликована: Фев. 23, 2025

Endothelial dysfunction (ED) is characterized by an imbalance between vasodilatory and vasoconstrictive factors, leading to impaired vascular tone, thrombosis, inflammation. These processes are critical in the development of cardiovascular diseases (CVDs) such as atherosclerosis, hypertension ischemia/reperfusion injury (IRI). Reduced nitric oxide (NO) production increased oxidative stress key contributors ED. Aging further exacerbates ED through mitochondrial oxidative/nitrosative stress, heightening CVD risk. Antioxidant systems like superoxide-dismutase (SOD), glutathione-peroxidase (GPx), thioredoxin/thioredoxin-reductase (Trx/TXNRD) pathways protect against stress. However, their reduced activity promotes ED, vulnerability IRI. Metabolic syndrome, comprising insulin resistance, obesity, hypertension, often accompanied Specifically, hyperglycemia worsens endothelial damage promoting Obesity leads chronic inflammation changes perivascular adipose tissue, while associated with increase The NLRP3 inflammasome plays a significant role being triggered factors reactive oxygen nitrogen species, ischemia, high glucose, which contribute inflammation, injury, exacerbation Treatments, N-acetyl-L-cysteine, SGLT2 or inhibitors, show promise improving function. Yet complexity suggests that multi-targeted therapies addressing metabolic disturbances essential for managing CVDs syndrome.

Язык: Английский

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Liver fibrosis as a barometer of systemic health by gauging the risk of extrahepatic disease

Metabolism and Target Organ Damage, Год журнала: 2024, Номер 4(4)

Опубликована: Ноя. 15, 2024

This review article proposes the theory that liver fibrosis, abnormal accumulation of excessive extracellular matrix, is not just an indicator disease but also a negative reflection overall systemic health. Liver fibrosis poses heavy financial burden on healthcare systems worldwide and can develop due to chronic from various causes, often sustained inflammation. may generate symptoms become apparent only when it reaches stage cirrhosis associated with clinically significant portal hypertension leads decompensation events or promotes development hepatocellular carcinoma. While viral hepatitis alcohol consumption were once primary causes featuring this role now increasingly taken over by metabolic dysfunction-associated steatotic (MASLD). In MASLD, endothelial dysfunction essential component in pathogenesis, promoting present cells other organs such as heart, lungs, kidneys. Accordingly, predictor liver-related outcomes, well all-cause mortality, cardiovascular risk, extrahepatic cancer. Physicians should be aware individuals seeking medical attention for reasons unrelated health have advanced fibrosis. Early identification these at-risk lead more comprehensive assessment use treatment options, both approved investigational, slow reverse progression

Язык: Английский

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Endothelial Dysfunction in Keloid Formation and Therapeutic Insights

Journal of Investigative Dermatology, Год журнала: 2025, Номер unknown

Опубликована: Март 1, 2025

Язык: Английский

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CMTM3 regulates vascular endothelial cell dysfunction by influencing pulmonary vascular endothelial permeability and inflammation in ARDS

Frontiers in Immunology, Год журнала: 2025, Номер 16

Опубликована: Март 24, 2025

Introduction CMTM3 is a member of the human chemokine-like factor superfamily. The mechanistic role in acute respiratory distress syndrome (ARDS) not known. This study investigated progression ARDS and its impact on function vascular endothelial cells. Methods modeling umbilical cells (HUVECs) was performed by treating with lipopolysaccharide (LPS) or hypoxia/reoxygenation. We assessed expression levels LPS- hypoxia/reoxygenation-stimulated HUVEC Furthermore, we permeability inflammatory response under conditions using overexpression(adCMTM3) knockdown(shCMTM3). Concurrently, generated knockout (CMTM3ko) mice evaluated differences pulmonary permeability, lung injury, survival rates between CMTM3ko-ARDS WT-ARDS model mice. Results HUVECs stimulated LPS hypoxia/reoxygenation showed significantly higher compared to control group (p<0.05). Compared adsham-HUVECs, adCMTM3-HUVECs demonstrated cellular (p<0.05) as well IL-6 TNF-α Conversely, shCMTM3-HUVECs reduced In vivo experiments that CMTM3-knockout exhibited (p=0.0194) injury wild-type Discussion These findings played critical development influencing inflammation. Therefore, potential therapeutic target ARDS.

Язык: Английский

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Biophysiochemically favorable, antithrombotic and pro-endothelial coordination compound nanocoating of copper (II) with protocatechuic acid & nattokinase on flow-diverting stents

Colloids and Surfaces B Biointerfaces, Год журнала: 2025, Номер 249, С. 114509 - 114509

Опубликована: Янв. 14, 2025

Язык: Английский

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Development of a recombinant Ang1 variant with enhanced Tie2 binding and its application to attenuate sepsis in mice

Science Advances, Год журнала: 2025, Номер 11(3)

Опубликована: Янв. 15, 2025

The angiopoietin (Ang)–Tie axis, critical for endothelial cell function and vascular development, is a promising therapeutic target treating disorders inflammatory conditions like sepsis. This study aimed to enhance the binding affinity of recombinant Ang1 variants Tie2 explore their potential. Structural insights from Ang1-Tie2 complex enabled identification key residues within receptor domain (RBD) interaction. Molecular dynamics simulations revealed that Met 436 Arg (M436R) Ala 451 Asp (A451D) could improve Ang1’s affinity. One variant, Ang1-RBD A451D , demonstrated 100-fold increase compared wild type. Cellular assays enhanced phosphorylation, promoting migration tube formation. In vivo, this variant effectively reduced cytokines attenuated organ damage in septic mice. These findings highlight as candidate diseases, offering notable clinical potential mitigating sepsis-related dysfunction.

Язык: Английский

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Promotion Mechanisms of Stromal Cell-Mediated Lung Cancer Development Within Tumor Microenvironment

Cancer Management and Research, Год журнала: 2025, Номер Volume 17, С. 249 - 266

Опубликована: Фев. 1, 2025

Abstract: Lung cancer, with its high incidence and mortality rates, has garnered significant attention in the medical community. The tumor microenvironment (TME), composed of cells, stromal extracellular matrix, surrounding blood vessels, other signaling molecules, plays a pivotal role development lung cancer. Stromal cells within TME hold potential as therapeutic targets for cancer treatment. However, precise comprehensive mechanisms by which contribute to progression have not been fully elucidated. This review aims explore through promote development, particular focus on how immune tumor-associated fibroblasts, endothelial suppression, inflammation, angiogenesis. goal is provide new insights strategies diagnosis treatment Keywords: microenvironment, cancer-associated

Язык: Английский

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PFOS and Its Substitute OBS Cause Endothelial Dysfunction to Promote Atherogenesis in ApoE^–/– Mice

Environment & Health, Год журнала: 2025, Номер unknown

Опубликована: Фев. 11, 2025

Perfluorooctanesulfonate (PFOS), an emerging contaminant with widespread concern, has been associated the pathogenesis of atherosclerosis (AS). As a substitute for PFOS, sodium p-perfluorous nonenoxybenzenesulfonate (OBS) is extensively utilized in various applications and detected human blood. However, its potential health risk AS remain unclear. In this study, we investigated comparative impacts PFOS OBS on endothelial dysfunction atherogenesis. vivo Apolipoprotein E knockout (ApoE–/–) mice were exposed to 0.4 or 4 mg/L PFOS/OBS 12 weeks. We found that dyslipidemia developed more rapidly OBS-exposed than PFOS-exposed mice. exhibited higher enrichment capacity both blood aortic tissues OBS. Remarkably, induced pronounced inflammatory response caused significant disruption barrier aorta ApoE–/– compared PFOS. vitro experiments showed OBS, at same exposure concentrations durations as (0.1–20 μmol/L, 48 h), effectively inhibited cell viability umbilical vein cells (HUVECs), levels lactate dehydrogenase (LDH) release, enhanced adhesion between HUVECs monocytes. Both activate NF-κB signaling pathway upregulate expression factors. Notably, use but not was shown disrupt junctions increase permeability by activating MAPK/ERK pathway. Our findings suggest may lead have greater impact presenting risks cardiovascular diseases.

Язык: Английский

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Roadmap for alleviating the manifestations of ageing in the cardiovascular system

Nature Reviews Cardiology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 19, 2025

Язык: Английский

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