Walnut oil as a dietary intervention for atherosclerosis: Efficacy and mechanistic pathways

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Год журнала: 2025, Номер 1870(4), С. 159607 - 159607

Опубликована: Март 8, 2025

Язык: Английский

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A Systematic Review of Endothelial Dysfunction in Chronic Venous Disease—Inflammation, Oxidative Stress, and Shear Stress

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(8), С. 3660 - 3660

Опубликована: Апрель 12, 2025

Chronic venous disease (CVD) is among the most common diseases in industrialized countries and has a significant socioeconomic impact. The diversity of clinical symptoms manifestations CVD pose major challenges routine diagnosis treatment. Despite high prevalence huge number surgical interventions performed every day, substantial proportion etiopathogenesis remains unclear. There are several widely advocated generally valid theories “peri-capillary fibrin cuffs” “white cell trapping hypothesis”, which consider role reflux/obstruction, inflammation, vascular remodeling, hemodynamic changes, genetic social risk factors. specific provoking factors for development reflux: incompetence valve system, inflammation wall, hypertension. Over past few years, increasing scientific data demonstrated link between oxidative stress, endothelial dysfunction, inflammation. High levels oxidants persistent can cause cumulative changes hemodynamics, resulting permanent irreversible damage to microcirculation cells. Production reactive oxygen species expression inflammatory cytokines adhesion molecules involved vicious cycle wall remodeling. interaction ROS, particular, superoxide anion radical, with nitric oxide leads decrease NO bioavailability, followed by initiation prolonged vasoconstriction hypoxia impairment tone. This review addresses ED, oxidative, stress mediation. Based on predefined inclusion exclusion criteria, we conducted systematic published articles using PubMed, PMC Europe, Scopus, WoS, MEDLINE, Google Scholar databases interval from 24 April 2002 1 2025. current included studies (n = 197) articles, including new reviews, updates, grey literature, were evaluated according eligibility criteria. selection process was standardized form PRISMA rules, manual search databases, double-check ensure transparent complete reporting reviews. Studies had report quantitative assessments relationship shear chronic disease.

Язык: Английский

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Investigation of the mechanism of hypertension caused by BTKi in the treatment of hematologic diseases

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Май 15, 2025

Bruton’s tyrosine kinase inhibitors (BTKis) have made substantial impacts on the treatment of B-cell malignancies like chronic lymphocytic leukemia (CLL) and small lymphoma (SLL). Therapeutic benefits aside, clinical use BTKis comes with several side effects, which hypertension (HTN) is quite common serious significant concern. The present article will discuss mechanisms by causes outline strategies for managing condition within clinic. Studies indicate that using interferes BTK’s central role receptor (BCR) signaling cascade multiple downstream pathways PI3K/Akt, MAPK, NF-κB. These changes contribute to endothelial dysfunction, increased oxidative stress, vascular constriction, all are implicated in development hypertension. Of special concern stress (OS) directly related decreased nitric oxide (NO) production, a finding becomes particularly relevant during initiation BTKi therapy. Also, affect tone regulation activating Notch RhoA/ROCK pathways, leading vasoconstriction advancement In light possibility BTKi-induced might jeopardize tolerability patient outcomes, this review proposes multimodal management condition, including careful monitoring blood pressure, individualized antihypertensive treatment, possible modifications dosing BTKis. Future investigations should look into specific molecular underpinning due as well effects various regimens improvement cardiovascular profile affected individuals.

Язык: Английский

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Characterizing hub biomarkers for metabolic-induced endothelial dysfunction and unveiling their regulatory roles in EndMT through RNA sequencing and machine learning approaches

Frontiers in Cardiovascular Medicine, Год журнала: 2025, Номер 12

Опубликована: Май 15, 2025

Background Metabolic disorder and endothelial dysfunction (ED) are key events in the development pathophysiology of atherosclerosis associated with an elevated risk Cardiovascular disease (CVD). The remains incompletely understood. Methods Leftover serum samples were collected stored at −20 °C until study. Serum specimens mixed to obtain pooled high glucose (GLU group) (11.97 ± 2.09 mmol/L); low-density lipoprotein (LDL [3.465 (3.3275, 3.6425 mmol/L)]; triglycerides (1.15 0.35 mmol/L) (TG group); Subsequently, Human umbilical vein cells (HUVECs) exposed culture media supplemented these or control for 72 h. Whole transcriptome sequencing was performed characterize gene expression profiles data analyzed using GSEA, GO, KEGG. qPCR used validate expression. Results A total 306 mRNAs 523 lncRNAs identified as differentially expressed GLU group, 335 471 LDL 364 562 TG compared group. These genes primarily involved inflammation, lipid metabolism, EndMT pathways. By integrating mRNA curated EndMT-related sets from KEGG, dbEMT2.0 databases, we 52 under metabolic stress conditions. Utilizing machine learning techniques, established EndMT-associated diagnostic signature comprising CD36, ISG15, HSPB2, IRS2 diagnosis AS, which achieved AUC 0.997. model subsequently validated across three independent external cohorts (GSE43292, GSE28829, GSE163154), it consistently demonstrated strong performance, values 0.958, 0.808, 0.884, respectively. ceRNA networks constructed related including LINC002381, VIM-AS1, ELF-AS1 significantly upregulated peripheral blood samples. Conclusions This study novel biomarkers ED. findings may provide both a potential biomarker therapeutic target prevention treatment CAD.

Язык: Английский

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Suppressing endothelial senescence: A comprehensive analysis of metformin's mechanisms and implications

Life Sciences, Год журнала: 2025, Номер unknown, С. 123730 - 123730

Опубликована: Май 1, 2025

Язык: Английский

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Adaptation of mitochondrial bioenergetics to coenzyme Q deficiency in human endothelial cells after chronic exposure to bisphosphonates

Scientific Reports, Год журнала: 2025, Номер 15(1)

Опубликована: Май 22, 2025

Abstract Nitrogen-containing bisphosphonates (N-BPs), widely used in bone disease therapy, inhibit the mevalonate pathway, which affects coenzyme Q (CoQ) biosynthesis and may compromise mitochondrial function, particularly endothelial cells where oxidative stress dysfunction contribute to cardiovascular disease. This study examined effects of chronic six-day exposure human N-BPs on bioenergetic functions, focusing drug-induced CoQ (mtCoQ) deficiency. Compared with mitochondria control cells, those treated 5 µM alendronate or 1 zoledronate presented a significant 45–50% decrease total mtCoQ pool, loss reduced (mtCoQH 2 ) antioxidant elevated protein superoxide dismutase (SOD2) uncoupling (UCP2) levels. Exposing also led an overall reduction substrate oxidation, except for increased fatty acid oxidation. Additionally, N-BP-treated decreased respiratory rates, membrane potential, ATP synthesis efficiency, H O production resulting from during oxidation complex I (CI) CII substrates. N-BP-induced deficiency resulted rearranged chain supercomplexes, downregulation III + IV supercomplex, CII, CIII, CV levels activities. Despite -heme levels, maximal CIV activity remained unaffected mitochondria. These findings highlight role disrupting redox homeostasis associated functions

Язык: Английский

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Metabolic Rewiring in Calcific Aortic Valve Disease: It Goes Beyond Immunometabolism

Arteriosclerosis Thrombosis and Vascular Biology, Год журнала: 2025, Номер unknown

Опубликована: Май 29, 2025

Язык: Английский

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