Molecular hydrogen reduces mean and systolic blood pressure in various forms of hypertension, as well as inflammatory processes in lung tissue, in Wistar rats DOI
Marina S Artemieva, Т. А. Куропаткина, В. В. Шишкина

et al.

Российский физиологический журнал им  И  М  Сеченова, Journal Year: 2024, Volume and Issue: 110(10), P. 1666 - 1682

Published: Dec. 29, 2024

Molecular hydrogen demonstrates antioxidant and anti-inflammatory properties. It has been shown to have a protective effect in several cardiovascular diseases. The aim of this work was study the breathing atmospheric air containing 4% on degree development monocrotaline-induced pulmonary hypertension associated lung tissue inflammation, as well severity renovascular Wistar rats. Methods. Monocrotaline-induced (MCT-PH) used model small circle hypertension. Three groups animals were experiment: "Control" – injected with monocrotaline solvent, "MCT-Control" "MCT-H2" MCT once. breathed for 21 days, group hydrogen. Inhalations kept constant until days. On day 21, haemodynamic parameters measured under urethane anesthesia samples fixed subsequent morphological analysis. Renovascular 1R1С (RVH) systemic There two RVH-C rats RVH-H2 During experiment, systolic blood pressure (SBP) renal excretory function assessed. 28, anesthesia. Results. In model, had no symptoms hypertension, but decreased mean (MBP), SBP markers connective remodeling lungs, TGF-β MMP-9, resulted tryptase secretion mast cell counts. RVG MBP, function. Conclusion. Inhalation reduces MBP both models arterial inflammatory process, regulates phenotypic functional status cells inhibits activity profibrotic factors MCT-PH. is likely that central action combined its anti-fibrotic effects.

Language: Английский

Pyroptosis in health and disease: mechanisms, regulation and clinical perspective DOI Creative Commons
Yifan Liu,

Renjie Pan,

Yuzhen Ouyang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: Sept. 20, 2024

Language: Английский

Citations

37
Exercise Training Alleviates Cardiac Fibrosis through Increasing Fibroblast Growth Factor 21 and Regulating TGF-β1-Smad2/3-MMP2/9 Signaling in Mice with Myocardial Infarction DOI Open Access
Yixuan Ma,

Yixin Kuang,

Wenyan Bo

et al.

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(22), P. 12341 - 12341

Published: Nov. 15, 2021

Exercise training has been reported to alleviate cardiac fibrosis and ameliorate heart dysfunction after myocardial infarction (MI), but the molecular mechanism is still not fully clarified. Fibroblast growth factor 21 (FGF21) exerts a protective effect on infarcted heart. This study investigates whether exercise could increase FGF21 protein expression regulate transforming factor-β1 (TGF-β1)-Smad2/3-MMP2/9 signaling pathway following MI. Male wild type (WT) C57BL/6J mice Fgf21 knockout (Fgf21 KO) were used establish MI model subjected five weeks of different types training. Both aerobic (AET) resistance (RET) significantly alleviated fibrosis, up-regulated expression, inhibited activation TGF-β1-Smad2/3-MMP2/9 collagen production, meanwhile, enhanced antioxidant capacity reduced cell apoptosis in In contrast, weakened cardioprotective effects AET vitro, fibroblasts (CFs) isolated from neonatal hearts treated with H2O2 (100 μM, 6 h). Recombinant human (rhFGF21, 100 ng/mL, 15 h) and/or 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR, 1 mM, H2O2-induced pathway, promoted CFs production. conclusion, increases inactivates alleviates oxidative stress, apoptosis, finally improves function plays an important role anti-fibrosis

Language: Английский

Citations

86
Gasdermin D-mediated pyroptosis in myocardial ischemia and reperfusion injury: Cumulative evidence for future cardioprotective strategies DOI Creative Commons
Panat Yanpiset, Chayodom Maneechote,

Sirawit Sriwichaiin

et al.

Acta Pharmaceutica Sinica B, Journal Year: 2022, Volume and Issue: 13(1), P. 29 - 53

Published: Aug. 14, 2022

Cardiomyocyte death is one of the major mechanisms contributing to development myocardial infarction (MI) and ischemia/reperfusion (MI/R) injury. Due limited regenerative ability cardiomyocytes, understanding cardiomyocyte necessary. Pyroptosis, regulated programmed cell pathways, has recently been shown play important roles in MI MI/R Pyroptosis activated by damage-associated molecular patterns (DAMPs) that are released from damaged cells activate formation an apoptosis-associated speck-like protein containing a CARD (ASC) interacting with NACHT, LRR, PYD domains-containing 3 (NLRP3), resulting caspase-1 cleavage which promotes activation Gasdermin D (GSDMD). This pathway known as canonical pathway. GSDMD also be non-canonical during injury via caspase-4/5/11. Suppression provide cardioprotection against Although effects or on pyroptosis have previously discussed, knowledge concerning these settings remains limited. In this review, evidence vitro, vivo, clinical studies focusing cardiac comprehensively summarized discussed. Implications review will help pave way for new therapeutic target ischemic heart disease.

Language: Английский

Citations

45
Cardiac Remodeling in Heart Failure: Role of Pyroptosis and Its Therapeutic Implications DOI Creative Commons

Ruoning Chai,

Wenjing Xue,

Shuqing Shi

et al.

Frontiers in Cardiovascular Medicine, Journal Year: 2022, Volume and Issue: 9

Published: April 18, 2022

Pyroptosis is a kind of programmed cell death closely related to inflammation. The pathways that mediate pyroptosis can be divided into the Caspase-1-dependent canonical pathway and Caspase4/5/11-dependent non-canonical pathway. most significant difference from other rapidly causes rupture plasma membrane, expansion, dissolution release contents large number inflammatory factors, send pro-inflammatory signals adjacent cells, recruit cells induce responses. Cardiac remodeling basic mechanism heart failure (HF) core pathophysiological research on underlying mechanism. A studies have shown cause cardiac fibrosis, hypertrophy, cardiomyocytes death, myocardial dysfunction, excessive inflammation, remodeling. Therefore, targeting has good prospect in improving HF. In this review, molecular summarized, relationship between HF analyzed in-depth, potential therapy improve adverse discussed, providing some ideas for study

Language: Английский

Citations

43
Epigenetic regulation of diverse regulated cell death modalities in cardiovascular disease: Insights into necroptosis, pyroptosis, ferroptosis, and cuproptosis DOI Creative Commons
Cong Chen, Jie Wang,

Shan Zhang

et al.

Redox Biology, Journal Year: 2024, Volume and Issue: 76, P. 103321 - 103321

Published: Aug. 19, 2024

Cell death constitutes a critical component of the pathophysiology cardiovascular diseases. A growing array non-apoptotic forms regulated cell (RCD)-such as necroptosis, ferroptosis, pyroptosis, and cuproptosis-has been identified is intimately linked to various conditions. These RCD are governed by genetically programmed mechanisms within cell, with epigenetic modifications being common crucial regulatory method. Such include DNA methylation, RNA histone acetylation, non-coding RNAs. This review recaps roles modifications, RNAs in diseases, well which regulate key proteins involved death. Furthermore, we systematically catalog existing pharmacological agents targeting novel their action article aims underscore pivotal role precisely regulating specific pathways thus offering potential new therapeutic avenues that may prove more effective safer than traditional treatments.

Language: Английский

Citations

8
Hydrogen combined with tetrandrine attenuates silica-induced pulmonary fibrosis via suppressing NF-kappaB/NLRP3 signaling pathway-mediated epithelial mesenchymal transition and inflammation DOI Creative Commons
Juan Li, Ping Cui,

Jing Hua

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 138, P. 112563 - 112563

Published: June 29, 2024

Silicosis is a progressive disease characterized by interstitial fibrosis resulting from inhalation of silica particles, and currently lacks specific treatment. Hydrogen (H

Language: Английский

Citations

7
The Role of NLRP3 Inflammasome in Diabetic Cardiomyopathy and Its Therapeutic Implications DOI Creative Commons
Kai Ding, Chao Song, Heng-Jing Hu

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2022, Volume and Issue: 2022, P. 1 - 19

Published: Sept. 6, 2022

Diabetic cardiomyopathy (DCM) is a serious complication of diabetes mellitus (DM). However, the precise molecular mechanisms remain largely unclear, and it still challenging disease to diagnose treat. The nucleotide-binding oligomerization domain leucine-rich repeat pyrin 3 (NLRP3) inflammasome critical part innate immune system in host defend against endogenous danger pathogenic microbial infections. Dysregulated NLRP3 activation results overproduction cytokines, primarily IL-1β IL-18, eventually, inflammatory cell death-pyroptosis. A series studies have indicated that participates development DCM, corresponding interventions could mitigate progression. Accordingly, this narrative review aimed at briefly summarizing cell-specific role DCM provides novel insights into developing therapeutic strategies targeting inflammasome.

Language: Английский

Citations

24
Effects of Molecular Hydrogen in the Pathophysiology and Management of Cardiovascular and Metabolic Diseases DOI Creative Commons
Ram B. Singh, Zuzana Sumbalová, Ghizal Fatima

et al.

Reviews in Cardiovascular Medicine, Journal Year: 2024, Volume and Issue: 25(1), P. 33 - 33

Published: Jan. 22, 2024

Diet and lifestyle choices, notably the Western-type diet, are implicated in oxidative stress inflammation, factors that elevate risk of cardiovascular diseases (CVDs) type 2 diabetes mellitus (T2DM). In contrast, Mediterranean rich antioxidants, appears to have protective effects against these risks. This article highlights dual role diet generating molecular hydrogen (H2) gut, H2's subsequent influence on pathophysiology prevention CVD T2DM. Dietary fiber, flavonoids, probiotics contribute production liters H2 functioning as antioxidants neutralize free radicals dampen inflammation. last two decades, mounting evidence has demonstrated both endogenously produced exogenously administered H2, whether via inhalation or H2-rich water (HRW), potent anti-inflammatory across a wide range biochemical pathophysiological processes. Recent studies indicate can hydroxyl nitrosyl radicals, acting cellular antioxidant, thereby reducing inflammation—leading significant decline CVDs metabolic diseases. Clinical experimental research support therapeutic potential interventions such HRW managing However, larger necessary verify therapy management chronic

Language: Английский

Citations

5
Hydrogen gas inhalation ameliorates cardiac remodelling and fibrosis by regulating NLRP3 inflammasome in myocardial infarction rats DOI
Chaoqun Nie,

Rentong Zou,

Shuang Pan

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2021, Volume and Issue: 25(18), P. 8997 - 9010

Published: Aug. 16, 2021

Abstract It is noteworthy that prolonged cardiac structural changes and excessive fibrosis caused by myocardial infarction (MI) seriously interfere with the treatment of heart failure in clinical practice. Currently, there are no effective practical means either prevention or treatment. Thus, novel therapeutic approaches critical for long‐term quality life individuals ischaemia. Herein, we aimed to explore protective effect H 2 , a gas signal molecule anti‐oxidative stress anti‐inflammatory effects, on remodelling MI rats, its possible mechanism. First, successfully established model which were then exposed inhalation 2% concentration 28 days (3 hours/day). The results showed hydrogen can significantly improve function reduce area fibrosis. In vitro experiments further proved hypoxia‐induced damage cardiomyocytes alleviate angiotensin II‐induced migration activation fibroblasts. conclusion, herein, illustrated first time ameliorates infarction‐induced rats exert mainly through inhibiting NLRP3‐mediated pyroptosis.

Language: Английский

Citations

29
Hydrogen decreases susceptibility to AngII-induced atrial fibrillation and atrial fibrosis via the NOX4/ROS/NLRP3 and TGF-β1/Smad2/3 signaling pathways DOI Creative Commons

Bin‐Mei Zhang,

Jingxiu Hou,

Jia‐Ren Liu

et al.

PLoS ONE, Journal Year: 2025, Volume and Issue: 20(1), P. e0310852 - e0310852

Published: Jan. 8, 2025

Atrial fibrillation (AF) represents the commonly occurring cardiac arrhythmia and main factor leading to stroke heart failure. Hydrogen (H 2 ) is a gaseous signaling molecule that has effects of anti-inflammation antioxidation. Our study provides evidence hydrogen decreases susceptibility AngII-mediated AF together with atrial fibrosis. Following continuous AngII administration for 28-day period, AngII+H treated rats showed decreased AF, decrease in fibrosis, ROS myocytes, an inhibition NLRP3 inflammasome activation, improvement electrical remodeling, proliferation migration fibroblasts. We further found regulates activation thus improves Ca 2+ handling IKAch IKur by inhibiting activity NOX4 vivo. In addition, was involved fibrosis through TGF-β1/Smad2/3 pathway suppressing TGF-β1 secretion findings suggest important preventing treating suggesting could be used as candidate way prevent treat AF.

Language: Английский

Citations

0