Causal relationship between antihypertensive drugs and Hashimoto’s thyroiditis: a drug-target Mendelian randomization study DOI Creative Commons
Bing Cui,

Aqin Chen,

Chengcheng Xu

et al.

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: Oct. 7, 2024

Introduction and objectives Recent studies have indicated a potential association of hypertension with Hashimoto’s thyroiditis (HT) other autoimmune diseases, yet the impact antihypertensive drugs on HT risk is not well understood. Methods We employed drug-target Mendelian randomization approach to investigate prolonged 9 classes medications susceptibility in European Asian populations. Genetic variants close or within genes associated drug targets systolic blood pressure (SBP) were utilized mimic effects medications. focused linked lower coronary artery disease for our main analysis. gathered genetic data SBP from comprehensive genome-wide available groups. For supplementary analysis, we used expression quantitative trait loci (eQTLs) related target as proxies. Results Our analysis revealed that use calcium channel blockers (CCBs) reduced both (OR [95% CI]: 0.96 [0.95 0.98] per 1 mmHg decrease SBP; p = 3.51×10 -5 ) populations 0.28 [0.12, 0.66]; 3.54×10 -3 ). Moreover, genetically mimicking loop diuretics 0.94 [0.91, 0.97]; 3.57×10 thiazide (0.98 [0.96, 0.99]; 3.83×10 showed significant decreased only population. These outcomes confirmed when eQTLs represent Conclusion The study suggests CCBs could potentially reduce different Additional research needed assess feasibility repurposing prevention HT.

Language: Английский

Pathophysiology of Angiotensin II-Mediated Hypertension, Cardiac Hypertrophy, and Failure: A Perspective from Macrophages DOI Creative Commons
Kelly Carter,

Eshan Shah,

Jessica Waite

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(23), P. 2001 - 2001

Published: Dec. 4, 2024

Heart failure is a complex syndrome characterized by cardiac hypertrophy, fibrosis, and diastolic/systolic dysfunction. These changes share many pathological features with significant inflammatory responses in the myocardium. Among various regulatory systems that impact on these heterogeneous processes, angiotensin II (Ang II)-activated macrophages play pivotal role induction of subcellular defects adverse remodeling during progression heart failure. Ang stimulates via its AT1 receptor to release oxygen-free radicals, cytokines, chemokines, other mediators myocardium, upregulates expression integrin adhesion molecules both monocytes endothelial cells, leading monocyte-endothelial cell-cell interactions. The transendothelial migration monocyte-derived exerts biological effects proliferation fibroblasts, deposition extracellular matrix proteins, perivascular/interstitial development hypertension, hypertrophy Inhibition macrophage activation using antagonist or depletion from peripheral circulation has shown inhibitory II-induced vascular myocardial injury. purpose this review discuss current understanding maladaptive dysfunction, particularly focusing molecular signaling pathways involved macrophages-mediated In addition, challenges remained translating findings treatment patients are also addressed.

Language: Английский

Citations

3
Mechanotransduction in the Perivascular Adipose Tissue DOI
Stephanie W. Watts, Teresa Krieger-Burke, Rance Nault

et al.

Arteriosclerosis Thrombosis and Vascular Biology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 13, 2025

Perivascular adipose tissue is of compelling interest when considering mechanotransduction. Because its location around a vessel, perivascular experiences from high (artery) to low (vein) pressures, pressures that are cyclical in nature. With blood pressure change, such as the elevation hypertension, question has been raised whether senses changes, evidenced by response can be genetic, structural, or mechanical Here, we briefly review following knowledge and data support ability both (mechano)sense (mechano)respond.

Language: Английский

Citations

0
Physicochemical and spectral investigation of interactions between hydralazine hydrochloride and dextrose in aqueous solutions DOI

Parveen Kumar,

Palak Ahir,

Sunaina Sharma

et al.

Journal of Molecular Liquids, Journal Year: 2025, Volume and Issue: unknown, P. 127250 - 127250

Published: Feb. 1, 2025

Language: Английский

Citations

0
The Role of the MAPK Signaling Pathway in Cardiovascular Disease: Pathophysiological Mechanisms and Clinical Therapy DOI Open Access
Xueyang Wang, Ruiqi Liu, Dan Liu

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(6), P. 2667 - 2667

Published: March 16, 2025

Cardiovascular disease (CVD) is a serious global health issue with high mortality rates worldwide. Despite the numerous advancements in study of CVD pathogenesis recent years, further summarization and elaboration specific molecular pathways are required. An extensive body research has been conducted to elucidate association between MAPK signaling pathway, which present all eukaryotic organisms, cardiovascular disease. This review aims provide comprehensive summary on over past five years. The primary focus four diseases: heart failure, atherosclerosis, myocardial ischemia–reperfusion injury, cardiac hypertrophy. will also address pathophysiological mechanisms diseases, objective proposing novel clinical treatment strategies for CVD.

Language: Английский

Citations

0
Impact of plant-derived antioxidants on heart aging: a mechanistic outlook DOI Creative Commons
Muneer Ahmed Khoso, Heng Liu, Tong Zhao

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: March 21, 2025

Heart aging involves a complex interplay of genetic and environmental influences, leading to gradual deterioration cardiovascular integrity function. Age-related physiological changes, including ventricular hypertrophy, diastolic dysfunction, myocardial fibrosis, increased arterial stiffness, endothelial are influenced by key mechanisms like autophagy, inflammation, oxidative stress. This review aims explore the therapeutic potential plant-derived bioactive antioxidants in mitigating heart aging. These compounds, often rich polyphenols, flavonoids, other phytochemicals, exhibit notable antioxidant, anti-inflammatory, cardioprotective properties. substances have intricate properties, ability scavenge ROS, enhance endogenous antioxidant defenses, regulate signaling pathways, impede fibrosis inflammation-promoting processes. By focusing on molecular linked cardiac aging, produced from plants provide significant promise reduce age-related decline improve general health. Through comprehensive analysis preclinical clinical studies, this work highlights associated with promising effects antioxidants. The findings may helpful for researchers identifying specific molecules preventive heart.

Language: Английский

Citations

0
Long-term Endurance Training as a Modulator for Preventing Cardiovascular Disease Risk in Obese Individuals DOI Creative Commons
Adi Pranoto, Shidqi Hamdi Pratama Putera, Dewangga Yudhistira

et al.

Physical Education Theory and Methodology, Journal Year: 2025, Volume and Issue: 25(2), P. 221 - 227

Published: March 30, 2025

Objectives. This study aimed to evaluate the long-term effects of endurance training as a modulator in prevention cardiovascular disease risk obese individuals. Materials and methods. used true experimental method with pretest-posttest control group design. Twenty-five women aged 20-30 years body fat percentage ≥30% were assigned (CNT) an exercise (EXC). The EXC underwent eight-week (three sessions per week) program (treadmill) lasting 40-60 minutes session. Blood pressure (BP), mean arterial (MAP), resting heart rate (RHR) measured using OMRON HBP-9030 digital tensiometer Polar H10 sensor at start (pre) after eight weeks (post) training. Results. Significant reductions systolic blood (SBP), diastolic (DBP), MAP, RHR detected between pre- post-endurance phases (all p ≤ 0.001). Additionally, notable decrease SBP, DBP, was observed groups 0.05). Conclusions. findings indicate effectiveness intervention, contributing consistent reduction women.

Language: Английский

Citations

0
Chronic Inflammation Linking Atherosclerosis to Cognitive Impairment: Multi-Target Mechanisms and Therapeutic Advances in Chinese Herbal Medicine DOI Creative Commons

Rumin Huang,

Xiangrui Zhang, Min Ni

et al.

Brain Behavior and Immunity Integrative, Journal Year: 2025, Volume and Issue: unknown, P. 100122 - 100122

Published: April 1, 2025

Language: Английский

Citations

0
Liposome of Phlorizin promote the repair of carotid atherosclerosis in rats by regulating inflammation and the Nrf2 signaling pathway DOI

Xiaoyu Wu,

Chuanbo Ding,

Xinglong Liu

et al.

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids, Journal Year: 2025, Volume and Issue: unknown, P. 159613 - 159613

Published: April 1, 2025

Language: Английский

Citations

0
Mechanism of Ershen Zhenwu Decoction in ameliorating chronic heart failure via JNK/MAPK-regulated apoptosis: insights from network pharmacology and experimental validation DOI Creative Commons
Yulong Liu, Xinyue Wang,

Maomao Zhang

et al.

Frontiers in Cardiovascular Medicine, Journal Year: 2025, Volume and Issue: 12

Published: April 22, 2025

Chronic heart failure (CHF) is a complex cardiovascular disease caused by different pathological mechanisms. Modern medicine has made advancements in CHF treatment; however, there are still many challenges. Ershen Zhenwu Decoction (ESZWD) Xin'an that been clinically applied for years and had good efficacy against CHF; its underlying mechanisms remain undetermined. Therefore, this study aims to investigate the primary molecular of ESZWD treatment elucidate multi-target multi-level mode action. The aim was main This employed network pharmacology approach analyze components core targets. Furthermore, targets were predicted develop protein-protein interaction (PPI) perform Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment analyses. Moreover, docking carried out validate binding between active ingredients key For vitro studies, myocardial cell injury models employed, immunofluorescence, RT-qPCR, Western blot, flow cytometry critical relevant signaling pathways specific regulatory Network identified 437 34 major components. Of these, 216 drug-disease intersection identified. PPI analysis following targets: STAT3, HSP90AA1, MAPK8, NFKB1, HIF1A, MMP9, PTGS2, BCL2L1, TLR4, ESR1. GO revealed these associated with exogenous stimuli responses, phosphorylation regulation, inflammatory response, protein tyrosine kinase activity. KEGG showed predominantly impacts cancer, apoptosis pathways, c-Jun N-terminal kinase/mitogen-activated (JNK/MAPK)-regulated being pathway. In analyses effectively inhibited JNK activation, modulated MAPK signaling, downregulated pro-apoptotic gene expression, significantly reduced cardiomyocyte rates, thus validating findings. Our shows paeoniflorin, acetylaconitine, cryptotanshinone bind proteins JNK/MAPK validation confirms drug serum from regulates pathway, supporting therapeutic potential CHF.

Language: Английский

Citations

0
Fraxin Alleviates Atherosclerosis by Inhibiting Oxidative Stress and Inflammatory Responses via the TLR4/PI3K/Akt Pathway DOI Creative Commons
Yaru Wang,

Bailing Wei,

Mingyang Leng

et al.

Current Issues in Molecular Biology, Journal Year: 2025, Volume and Issue: 47(5), P. 308 - 308

Published: April 27, 2025

Fraxin is a bioactive compound derived from Cortex Fraxini. It known for its diverse biological activities and numerous benefits, including anti-inflammatory, antioxidant, analgesic, antimicrobial, antiviral, immunomodulatory effects. Despite growing interest in natural compounds cardiovascular diseases Fraxin’s atheroprotective properties molecular targets have not yet been fully elucidated. To address this gap, our research employed an integrated approach combining network pharmacology, docking simulations, vitro validation to systematically unravel therapeutic mechanisms against atherosclerosis (AS). The results showed that 84 potential AS were predicted through public databases, the key target TLR4 was identified by protein–protein interaction analysis. GO enrichment KEGG pathway analysis revealed these significantly enriched PI3K-Akt oxidative stress responses pathways. Subsequently conducted studies validated modulates TLR4/PI3K/Akt signaling suppress reactive oxygen species generation downregulate pro-inflammatory cytokines Il1b, Il6, Tnf thereby slowing atherosclerotic disease advancement. This investigation methodically delineates underlying management, establishing scientific foundation translation into clinical practice.

Language: Английский

Citations

0