Left ventricular remodeling in normotensive Wistar rats exposed to intermittent hypoxia of different duration DOI Creative Commons

Yu. M. Kolesnyk,

M. Yu. Kolesnyk, O. V. Hancheva

и другие.

Pathologia, Год журнала: 2023, Номер 20(1), С. 5 - 13

Опубликована: Апрель 28, 2023

Intermittent hypoxia has been studied for many years as a promising non-pharmacological method of cardiovascular disease prevention. Hypoxic effects are accompanied by structural and functional changes in the myocardium. There is direct link between duration hypoxic exposures severity left ventricular myocardial remodeling. A range histochemical markers remodeling (cardiotrophin-1, titin, collagen type 1, annexin V) characterizing parenchymal-stromal relationships myocardium shown high informativeness prognostic value. The aim study was to examine cardiotrophin-1, V morphofunctional state ventricle heart experimental rats exposed intermittent 15-day (IH15) 60-day (IH60). Materials methods. modeled using 30 normotensive male Wistar rats, 7–8 months old, which were randomly assigned 3 groups 10 animals each: 1) INT – control group intact (196.3 ± 6.8 g); 2) IH15 (205.6 4.1 3) IH60 (201.1 5.5 g). compared varying duration: hypoxia. Experimental modeling 2 terms revealed number differences dependent on this factor through (blood pressure measurement, echocardiography) immunofluorescent studies. Results. Blood both range, but an increase systolic % diastolic 19 found (p < 0.05). In group, there significant decrease end-diastolic dimension 20 %, end-systolic 22 thickness posterior wall 44 interventricular septum 33 well mass 12 indicating concentric ventricle, development confirmed 76 relative that Along with these changes, volume 47 48 stroke 49 cardiac output 50 preserved ejection fraction While parameters characterized 17 23 15 higher than value At same time, 9 decreased 24 increased Also, 58 8 concentrations exceeded those IH15, namely: cardiotrophin-1 39 titin 70 1 60 130 Conclusions. forms hypertrophy according echocardiography findings; marker profile moderate resilient-elastic properties intensity cardiomyocyte death. Remodeling caused eccentric pattern severe hypertrophy, fibrosis associated apoptosis cardiomyocytes. Such may indicate initial stages maladaptation, increasing risk failure development.

Язык: Английский

Redox homeostasis in cardiac fibrosis: Focus on metal ion metabolism DOI Creative Commons
Zhenyu Liu,

Zhiyan Liu,

Li-Chan Lin

и другие.

Redox Biology, Год журнала: 2024, Номер 71, С. 103109 - 103109

Опубликована: Март 1, 2024

Cardiac fibrosis is a major public health problem worldwide, with high morbidity and mortality, affecting almost all patients heart disease worldwide. It characterized by fibroblast activation, abnormal proliferation, excessive deposition, distribution of extracellular matrix (ECM) proteins. The maladaptive process cardiac complex often involves multiple mechanisms. With the increasing research on fibrosis, redox has been recognized as an important part remodeling, imbalance in homeostasis can adversely affect function structure heart. metabolism metal ions essential for life, cells impair variety biochemical processes, especially redox. However, current ion still very limited. This review comprehensively examines effects (iron, copper, calcium, zinc) metabolism-mediated outlines possible therapeutic interventions, addresses ongoing challenges this rapidly evolving field.

Язык: Английский

Процитировано

17

Quercitrin improves cardiac remodeling following myocardial infarction by regulating macrophage polarization and metabolic reprogramming DOI Creative Commons

Congyong Liu,

Jungang Huang,

Junxiong Qiu

и другие.

Phytomedicine, Год журнала: 2024, Номер 127, С. 155467 - 155467

Опубликована: Фев. 19, 2024

The death and disability caused by myocardial infarction is a health problem that needs to be addressed worldwide, poor cardiac repair fibrosis after seriously affect patient recovery. Postmyocardial M2 macrophages of great significance for ventricular remodeling. Quercitrin (Que) common flavonoid in fruits vegetables has antioxidant, anti-inflammatory, antitumor other effects, but whether it role the treatment unclear. In this study, we constructed mouse model administered Que. We found through ultrasound Que administration improved ejection fraction reduced Staining heart sections detection marker protein levels revealed slowed infarction. Flow cytometry showed proportion was increased expression macrophage markers were Que-treated group. Finally, identified metabolomics reduces glycolysis, increases aerobic phosphorylation, alters arginine metabolic pathways, polarizing toward phenotype. Our research lays foundation future application cardiovascular diseases.

Язык: Английский

Процитировано

16

Targeted Mitochondrial Function for Cardiac Fibrosis: an Epigenetic Perspective DOI
Peng Liu, Zhenyu Liu,

Sui Mao

и другие.

Free Radical Biology and Medicine, Год журнала: 2025, Номер 228, С. 163 - 172

Опубликована: Янв. 2, 2025

Язык: Английский

Процитировано

1

Nitro-oleic acid alleviates inflammation and fibrosis by regulating macrophage polarization and fibroblast activation to improve cardiac function in MI mice DOI Creative Commons
Zhen Ma, Bingxin Huang,

Chenjun Yin

и другие.

International Immunopharmacology, Год журнала: 2025, Номер 146, С. 113710 - 113710

Опубликована: Янв. 1, 2025

Chronic heart failure, caused by myocardial fibrosis after acute infarction (AMI), remains a serious clinical problem that needs urgent resolution. Nitro-oleic acid (OA-NO2), an electrophilic nitro-fatty found in human plasma, is believed to regulate various pathophysiological functions, particularly anti-inflammation and anti-fibrosis. However, the role of OA-NO2 AMI unexplored. Thus, our aim was investigate whether could ameliorate post-myocardial fibrosis, improve cardiac function, elucidate its mechanism mice. In vivo experiments involved constructing mice model administering via subcutaneous osmotic minipumps. Echocardiography transmission electron microscope indicated can alleviate injury systolic function. Transcriptomics tissue suggested improved fibrosis. Immunohistochemistry qPCR results demonstrated OA-NO2's reduction accumulation extracellular matrix (Collagen I Collagen III). vitro showed remarkably suppressed activation fibroblasts myofibroblast transition induced transforming growth factor-β (TGF-β). Furthermore, inhibited expression α-SMA, collagen I, III TGF-β/smad2/3 signaling pathway. Immunofluorescence ELISA detection revealed not only alleviated but also reduced inflammation decreased inflammatory factors (TNF-α, IL-1β, IL-6, MCP-1). Mechanistically, significantly polarization LPS-induced macrophages into M1-type inhibiting NF-κB (P65) related pathways. Therefore, postmyocardial function myofibroblasts M1 macrophages.

Язык: Английский

Процитировано

1

Targeting Inflammation with Galectin-3 and PIIINP Modulation Among ST-Segment Elevation Acute Coronary Syndrome Patients Underwent Delayed Percutaneous Coronary Intervention DOI Creative Commons
Saskia Dyah Handari, Saifur Rohman, Djanggan Sargowo

и другие.

Biomedicines, Год журнала: 2025, Номер 13(2), С. 259 - 259

Опубликована: Янв. 21, 2025

Background/Objectives: ST-segment elevation acute coronary syndrome (STE-ACS) represents a significant global health challenge, with cardiac remodeling and fibrosis critically affecting recovery after percutaneous intervention (PCI). Colchicine, known for its anti-inflammatory effects, may regulate key fibrotic markers such as Procollagen III N-terminal Propeptide (PIIINP) Galectin-3. This study assesses colchicine’s effect on these biomarkers in STE-ACS patients undergoing delayed PCI. Methods: In this multicenter, randomized, double-blind trial, we examined impact Galectin-3 PIIINP 164 early or Patients received colchicine shortly hospital admission. Biomarker changes were evaluated at 24 h five days post-treatment using two-way ANOVA. Results: Clinical trials the PCI group revealed that levels decreased significantly day one (p < 0.01) further 0.0001), indicating Primary has benefits to inhibition of beyond add-on treatment. But, group, increased 0.01), but decrease observed by was not statistically significant. It is related treatment exceed implantation preventing remodeling. showed reduction 0.0001). Conclusions: Colchicine demonstrates novel efficacy PCI, increase sharp PIIINP, ability control fibrosis. positions breakthrough therapy improving outcomes intervention.

Язык: Английский

Процитировано

1

Takeda G protein–coupled receptor 5 (TGR5): an attractive therapeutic target for aging-related cardiovascular diseases DOI Creative Commons

Yufeng He,

Si-qi Liu, Yali Zhang

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Март 20, 2025

Aging is an independent risk factor for many chronic diseases, including cancer and cardiovascular, pulmonary, neurodegenerative diseases. In recent years, the mechanisms of aging-related cardiovascular diseases (CVDs) have been studied intensively. Takeda G protein-coupled receptor 5 (TGR5) a membrane bile acids that has found to play important role in various disease processes, such as inflammation, oxidative stress, metabolic disorders, all which contribute CVDs. this review, we summarise TGR5 CVDs propose attractive therapeutic target based on its mechanism involvement, may future drug design.

Язык: Английский

Процитировано

1

m6A control programmed cell death in cardiac fibrosis DOI
Zhenyu Liu,

Qing-Ye You,

Zhiyan Liu

и другие.

Life Sciences, Год журнала: 2024, Номер 353, С. 122922 - 122922

Опубликована: Июль 18, 2024

Язык: Английский

Процитировано

6

Galanin Coordinates Macrophage-Associated Fibro-Inflammatory Response and Mitochondrial Integrity in Myocardial Infarction Reperfusion Injury DOI Open Access
Lesia Savchenko, С. Б. Крамар, Nika Todua

и другие.

International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(11), С. 6211 - 6211

Опубликована: Июнь 5, 2024

Myocardial infarction activates an intense fibro-inflammatory reaction that is essential for cardiac remodeling and heart failure (HF). Bioactive peptide galanin plays a critical role in regulating cardiovascular homeostasis; however, its specific functional relevance post-infarction reprogramming remains obscure. Here, we show coordinates the trajectory mitochondrial integrity reperfusion injury. Aberrant deposition of collagen was associated with marked increase CD68-positive macrophage infiltration tissue mice subjected to myocardial ischemia/reperfusion (I/R) 14 days compared sham controls. Furthermore, found expression level marker M2 macrophages, CD206, significantly down-regulated I/R-challenged mice. In contrast, treatment started during phase blunted responses promoted CD206 I/R-remodeled hearts. addition, anti-apoptotic anti-hypertrophic effects were preservation promotion biogenesis. These findings depict as key arbitrator I/R injury offer promising therapeutic post-infarct complications.

Язык: Английский

Процитировано

3

Innovative Approaches to Boost Mesenchymal Stem Cells Efficacy in Myocardial Infarction Therapy DOI Creative Commons
Chuanfeng An, Yuan Zhao, Lipeng Guo

и другие.

Materials Today Bio, Год журнала: 2025, Номер 31, С. 101476 - 101476

Опубликована: Янв. 9, 2025

Stem cell-based therapy has emerged as a promising approach for heart repair, potentially regenerating damaged tissue and improving outcomes patients with disease. However, the efficacy of stem therapies remains limited by several challenges, including poor cell survival, low retention rates, integration, functional outcomes. This article reviews current enhancement strategies to optimize mesenchymal cardiac repair. Key approaches include optimizing delivery methods, enhancing engraftment, promoting functions through genetic molecular modifications, paracrine effects cells, leveraging biomaterials engineering techniques. By focusing on these techniques, paper highlights innovative that can transform into more viable effective treatment option The ongoing research technological advancements continue push boundaries, hoping make mainstream

Язык: Английский

Процитировано

0

Nanomaterials: Promising Tools for the Diagnosis and Treatment of Myocardial Infarction DOI Creative Commons

Yanmin Ge,

Longwen Wu, Sen Mei

и другие.

International Journal of Nanomedicine, Год журнала: 2025, Номер Volume 20, С. 1747 - 1768

Опубликована: Фев. 1, 2025

Abstract: Myocardial infarction (MI) is the leading cause of mortality from cardiovascular diseases. Rapid diagnosis and effective treatment are critical for improving patient prognosis. Although current diagnostic therapeutic approaches have made significant progress, they still face challenges such as ischemia-reperfusion injury, microcirculatory disorders, adverse cardiac remodeling, inflammatory responses. These issues highlight urgent need innovative solutions. Nanomaterials, with their diverse types, excellent physicochemical properties, biocompatibility, targeting capabilities, offer promising potential in addressing these challenges. Advances nanotechnology increasingly drawn attention to application nanomaterials both diagnosing treating myocardial infarction. We summarize pathophysiological mechanisms staging systematically review applications MI diagnosis, including detection biomarkers imaging techniques, well treatment, encompassing anti-inflammatory effects, antioxidant stress, inhibition fibrosis, promotion angiogenesis, conduction repair. analyze existing provide insights into future research directions Specifically, we discuss rigorous safety assessments, long-term efficacy studies, development robust strategies translating laboratory findings clinical practice. In conclusion, holds promise a new strategy Its enhance outcomes revolutionize care makes it an exciting area practical real-world settings. Keywords: infarction, nanomaterials, nanoparticles,

Язык: Английский

Процитировано

0