Mechanisms of inflammatory microenvironment formation in cardiometabolic diseases: molecular and cellular perspectives

Frontiers in Cardiovascular Medicine, Journal Year: 2025, Volume and Issue: 11

Published: Jan. 14, 2025

Cardiometabolic diseases (CMD) are leading causes of death and disability worldwide, with complex pathophysiological mechanisms in which inflammation plays a crucial role. This review aims to elucidate the molecular cellular within inflammatory microenvironment atherosclerosis, hypertension diabetic cardiomyopathy. In oxidized low-density lipoprotein (ox-LDL) pro-inflammatory cytokines such as Interleukin-6 (IL-6) Tumor Necrosis Factor-alpha (TNF-α) activate immune cells contributing foam cell formation arterial wall thickening. Hypertension involves activation renin-angiotensin system (RAS) alongside oxidative stress-induced endothelial dysfunction local mediated by T cells. cardiomyopathy, high-glucose environment leads accumulation advanced glycation end products (AGEs), activating Receptor for Advanced Glycation Endproducts (RAGE) triggering responses that further damage cardiac microvascular function. summary, different types metabolic cardiovascular diverse; understanding these deeply will aid developing more effective individualized treatment strategies.

Language: Английский

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Angiotensin III activates ERK1/2 mitogen activated protein kinases and proliferation of rat vascular smooth muscle cells

Journal of Receptors and Signal Transduction, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 12

Published: Jan. 13, 2025

The proliferative effects of angiotensin (Ang) II in vascular smooth muscle cells (VSMCs) through its ability to stimulate extracellular signal-regulated kinases 1 and 2 (ERK1/2) pathway have been established. main goal this study was explore whether Ang III induces ERK1/2 MAPK VSMC proliferation cultured Wistar VSMCs. Further, the actions were compared those observed VSMCs derived from spontaneously hypertensive rat (SHR). We hypothesized that will similar as induce cellular may be different isolated versus SHR rats. Time and/or concentration-dependent determined using western blot analysis DNA incorporation assay. results showed phosphorylation mediated by or concentration- time-dependent Moreover, less effective mediating seen induced AT1 receptors activation. synthesis via receptor a manner significant differences existed peptide's These indicate stimulates receptors. However, these pathways is reduced

Language: Английский

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Vascular Impairment, Muscle Atrophy, and Cognitive Decline: Critical Age-Related Conditions

Biomedicines, Journal Year: 2024, Volume and Issue: 12(9), P. 2096 - 2096

Published: Sept. 13, 2024

The triad of vascular impairment, muscle atrophy, and cognitive decline represents critical age-related conditions that significantly impact health. Vascular impairment disrupts blood flow, precipitating the mass reduction seen in sarcopenia neuronal function characteristic neurodegeneration. Our limited understanding intricate relationships within this hinders accurate diagnosis effective treatment strategies. This review analyzes interrelated mechanisms contribute to these conditions, with a specific focus on oxidative stress, chronic inflammation, impaired nutrient delivery. aim is understand common pathways involved suggest comprehensive therapeutic approaches. dysfunctions hinder circulation transportation nutrients, resulting characterized by atrophy weakness. dysfunction have negative physical quality life. Neurodegenerative diseases exhibit comparable pathophysiological affect motor functions. Preventive approaches encompass lifestyle adjustments, addressing integrated therapies improving muscular well-being. Better links can refine strategies yield better patient outcomes. study emphasizes complex interplay between dysfunction, degeneration, decline, highlighting necessity for multidisciplinary Advances domain promise improved diagnostic accuracy, more options, enhanced preventive measures, all contributing higher life elderly population.

Language: Английский

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Relationship Between Carotid Artery Remodeling Characteristics and Early Carotid Atherosclerosis

Journal of Ultrasound in Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 21, 2025

Objectives This study analyzed carotid artery remodeling characteristics in early atherosclerosis (ECAS). Methods The 1021 participants were evaluated using ultrasonography and categorized into three groups: Group A, 391 with increased intima‐media thickness (IMT); B, 300 atherosclerotic plaque only on the bulb (CB); control group (330 participants). ratios of diameters CB to those common ( D CCA ) internal ICA defined as index1 (CI 1 2 ). Results A had a higher , CI than controls P < .05). B smaller Logistic regression showed that was positive influencing factor for IMT (OR: 3.42, 95% CI: 1.74–6.70, .001), negative independent formation 0.11, 0.04–0.28, .001). Multiple linear vessel side significant influence β = 0.055, .05), while age, sex, body mass index, cerebrovascular risk factors no correlation CI. Conclusions IMT, however, formation. changes consistent remodeling. an ECAS, it affected by side, providing objective predictive parameter ECAS.

Language: Английский

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Hepatic Arterial Flow-Induced Portal Tract Fibrosis in Portal Hypertension: The Role of VCAM-1 and Osteopontin-Expressing Macrophages

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 6, 2025

ABSTRACT Background The liver undergoes significant hemodynamic changes during surgery, transplantation, or cirrhosis with portal hypertension(PH). hepatic artery buffer response(HABR), which compensates for reduced venous flow by increasing artery(HA) flow, is hypothesized to induce pathological tract remodeling. This study investigates the molecular mechanisms underlying this process. Methods PH was induced in Sprague-Dawley rats via partial vein ligation(PPVL). Structural evaluation(microCT), immune cell profiling, measurements, and transcriptomic analysis macrophages(Mϕ) from sham PPVL were conducted. Results MicroCT revealed decreased increased HA correlated pressure(r=0.799, p<0.01). A 2-fold increase fibrosis(p<0.001) observed α-SMA+ myofibroblasts rats. CD68+ Mϕ peaked at 10 days post-PPVL, their depletion significantly fibrosis(p<0.001), indicating critical roles of VCAM-1 elevated endothelium fibroblasts (PFs); neutralization collagen accumulation(p<0.05), Mϕ(46.3%, p<0.01), CD3+ T cells(18%, p<0.05). Mϕ-conditioned medium PFs(8-fold, p<0.001) enhanced PF migration, while knockdown effect (p<0.01). Single-cell RNA sequencing data(GSE171904) RNA-FISH interactions between osteopontin (Spp1)+ PFs, Spp1+ driving fibrosis. Spp1 co-culture fibrogenic markers, recombinant upregulated Col1a1, Fn1, Acta2 expression PFs. Conclusion Increased arterial endothelial cells PFs facilitates recruitment Mϕ, drive flow-mediated vascular remodeling These findings highlight flow-induced fibrosis as a key mechanism PH, potentially contributing disease progression decompensation. Synopsis Liver hypertension extracellular matrix accumulation macrophages. highlights how altered blood induces fibrosis, its potential role decompensation, identifies therapeutic targets advanced disease.

Language: Английский

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The role of AT-1 antagonist on wound healing in rats with hypertension and diabetes

Journal of Molecular Histology, Journal Year: 2025, Volume and Issue: 56(2)

Published: Feb. 8, 2025

Language: Английский

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The “Silent Enemy” Called Renal Artery Stenosis: A Mini-Review

Journal of Vascular Diseases, Journal Year: 2025, Volume and Issue: 4(1), P. 10 - 10

Published: March 11, 2025

Renal artery stenosis (RAS) is a vascular condition characterized by narrowing of one or both renal arteries, leading to reduced blood flow the kidneys, activation renin–angiotensin–aldosterone system (RAAS), and subsequent renovascular hypertension. Overactivation same cascade potentiates production angiotensin II, which induces systemic vasoconstriction, increases sodium water retention via aldosterone, activates sympathetic nervous system. Angiotensin II also implicated in endothelial dysfunction, oxidative stress, chronic inflammation, thus impairing remodeling arterial stiffness, all serve accelerate cardiovascular complications, such as left ventricular hypertrophy, heart failure, myocardial infarction. RAS usually due at least 90% cases atherosclerosis, typically affects older people with diabetes smoking risk factors. There are two types RAS: unilateral bilateral. Bilateral commonly associated flash pulmonary edema, life-threatening emergency alveolar space flooding can occur within minutes. remains asymptomatic until late stage complications hypertension, ischemic nephropathy, kidney disease. FMD tends create structural abnormalities artery, whereas atherosclerosis causes plaque formation dysfunction artery. Epidemiological surveys have revealed that prevalence ranges from 4% 53% especially high among patients disease, CKD. Diagnosis based on clinical suspicion supported imaging studies, including Doppler ultrasound, computed tomography angiography, magnetic resonance angiography. Early detection relies certain laboratory biomarkers, identifying high-risk patients. These markers would include increased plasma renin activity, elevated aldosterone-renin ratio, inflammatory markers, C-reactive protein endothelin-1. Treatment involve pharmacological approaches, RAAS inhibitors, beta-blockers, statins, interventional treatments, angioplasty stenting severe forms However, Cardiovascular Outcomes Atherosclerotic Lesions (CORAL) Trial showed most likely require medical therapy, intervention should be reserved for those uncontrolled progressive recurrent episodes edema. Other emerging therapies drug-eluting balloons, bioresorbable stents, gene-editing techniques, shown great promise few studies been conducted, although further evaluation needed. Despite these advances, there still gaps knowledge regarding patient stratification, biomarker validation, development personalized treatment strategies. This article reviews complexities its impact health. Future research therefore focus improving early diagnosis, optimizing selection intervention, developing new slow disease progression mitigate complications.

Language: Английский

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Cardiomyocyte regeneration after infarction: changes, opportunities and challenges

Molecular and Cellular Biochemistry, Journal Year: 2025, Volume and Issue: unknown

Published: March 17, 2025

Language: Английский

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A Novel Hidden Protein p-414aa Encoded by circSETD2(14,15 ) Inhibits Vascular Remodeling

Circulation, Journal Year: 2025, Volume and Issue: unknown

Published: March 18, 2025

BACKGROUND: Phenotypic switching of vascular smooth muscle cells (VSMCs), leading to neointimal hyperplasia, is a fundamental cause remodeling diseases such as atherosclerosis and hypertension. Novel hidden proteins encoded by circular RNAs play crucial roles in disease progression, yet their involvement has not been comprehensively studied. This study identifies novel protein derived from RNA VSMCs demonstrates its potential role regulating remodeling. METHODS: Cell proliferation assays were performed investigate the effects circSETD2(14,15 ) on VSMC proliferation. Techniques vector construction, immunoprecipitation–mass spectrometry, dual-luciferase reporter gene used confirm that protein, p-414aa. The interaction between p-414aa HuR (human antigen R) was validated with techniques coimmunoprecipitation, mass proximity ligation assay. Through experiments including sequencing immunoprecipitation, C-FOS (C-Fos proto-oncogene) mRNA revealed. hyperplasia assessed carotid artery model male mice. RESULTS: Overexpression inhibits phenotypic switching. p-414aa, ), interacts reduce stability, thereby suppressing ultimately inhibiting CONCLUSIONS: We uncover called CircSETD2(14,15 may serve therapeutic targets for diseases.

Language: Английский

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Is there a link between the abundance of nitrate-reducing bacteria and arterial hypertension? A systematic review

Nitric Oxide, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

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