Quantitating myocardial fibrosis using extracellular extravascular volume determined from computed tomography myocardial perfusion imaging DOI Creative Commons
Na Li, Xin Zhang, Jin Gu

et al.

BMC Medical Imaging, Journal Year: 2024, Volume and Issue: 24(1)

Published: Feb. 12, 2024

Abstract Purpose Both of extracellular extravascular volume (EEV) and fraction (ECV) were proposed to quantify enlargement myocardial interstitial space due myocardium loss or fibrosis. The study aimed investigate the feasibility using EEV derived from computed tomography (CT) perfusion imaging (VPCT) quantification with single-energy subtraction CT (ECV − SECT ) for quantifying Methods In this study, 17 patients suspected known coronary artery disease underwent examination a dual-source scanner. VPCT was dynamic whole-heart imaging, ECV _SECT calculated late-enhanced images 5 min after bolus contrast injection by subtracting noncontrast baseline. late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) used as reference. Results total, 11 73 segments exhibited positivity LGE CMR imaging. These classified into three groups according segments: fibrotic (group I, n = 73), nonfibrotic in LGE-positive II, 103), LGE-negative III, 80). , blood flow (MBF), (MBV) significantly differed among these (all P < 0.05). higher MBF, MBV lower than ones 0.01). independently affected There no significant correlation between . capability diagnose fibrosis equivalent that (area under curve: 0.798 vs. 0.806, 0.844). > 41.2% 10.3% indicated Conclusions is actually first-pass distribution can feasibly be Furthermore, diagnostic efficacy comparable

Language: Английский

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

Zhiyan Liu,

Li-Chan Lin

et al.

Redox Biology, Journal Year: 2024, Volume and Issue: 71, P. 103109 - 103109

Published: March 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.

Language: Английский

Citations

16
Quercitrin improves cardiac remodeling following myocardial infarction by regulating macrophage polarization and metabolic reprogramming DOI Creative Commons

Congyong Liu,

Jungang Huang,

Junxiong Qiu

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 127, P. 155467 - 155467

Published: Feb. 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.

Language: Английский

Citations

14
Targeted Mitochondrial Function for Cardiac Fibrosis: an Epigenetic Perspective DOI
Peng Liu, Zhenyu Liu,

Sui Mao

et al.

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: 228, P. 163 - 172

Published: Jan. 2, 2025

Language: Английский

Citations

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

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 146, P. 113710 - 113710

Published: Jan. 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.

Language: Английский

Citations

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

et al.

Biomedicines, Journal Year: 2025, Volume and Issue: 13(2), P. 259 - 259

Published: Jan. 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.

Language: Английский

Citations

1
m6A control programmed cell death in cardiac fibrosis DOI
Zhenyu Liu,

Qing-Ye You,

Zhiyan Liu

et al.

Life Sciences, Journal Year: 2024, Volume and Issue: 353, P. 122922 - 122922

Published: July 18, 2024

Language: Английский

Citations

5
Glucose-dependent insulinotropic polypeptide/glucagon-like peptide 1 receptor agonist tirzepatide promotes branched chain amino acid catabolism to prevent myocardial infarction in non-diabetic mice DOI
Mengya Chen, Nan Zhao,

Wenke Shi

et al.

Cardiovascular Research, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 30, 2025

A novel dual glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1 receptor agonist, tirzepatide (LY3298176, TZP), has been developed to treat Type 2 diabetes mellitus (T2DM). In ischaemic heart diseases, TZP is involved in cardiac metabolic processes. However, its efficacy safety treating failure (HF) following myocardial infarction (MI) remain uncertain. Herein, 12 week C57BL/6J mice were subjected MI surgery, followed by administration of TZP. The effects on function metabolism thoroughly assessed physiological, histological, cellular analyses. Downstream effectors screened through untargeted metabolomics analysis molecular docking. Construct a lower branched chain amino acid (BCAA) diet model determine whether TZP's cardioprotective effect associated with reducing BCAA levels. Our results demonstrated that reduced mortality MI, decreased the infarct area, attenuated cardiomyocyte necrosis. Pathological evaluation tissues increased fibrosis repair inflammatory infiltration. Mechanistically, uncovered positive correlation between catabolism pathway. docking verified could bind branched-chain keto dehydrogenase E1 subunit α (BCKDHA). BCKDHA phosphorylation at S293, enhanced catabolism, inhibited activation activating rapamycin (mTOR) signalling Furthermore, fed low-BCAA post-MI necrosis, repair, These further when used synergistically Taken together, our findings provide new perspectives unrecognized role protection. BCAA/mTOR pathway mice. Consequently, this study may present therapeutic options for patients HF.

Language: Английский

Citations

0
Myocardial Characterization on CT: Late Iodine Enhancement and Extracellular Volume DOI
Axel Bartoli, Chiara Gnasso, Anna Palmisano

et al.

Echocardiography, Journal Year: 2025, Volume and Issue: 42(2)

Published: Feb. 1, 2025

ABSTRACT Myocardial tissue characterization is fundamental in diagnosing, treating, and managing various cardiac diseases. In recent years, computed tomography (CCT) emerged as a valuable alternative to magnetic resonance (CMR) for myocardial characterization, with the possibility detect scar quantify extracellular volume fraction single CT study advantage of combined coronary arteries evaluation, shorter scanning time, less susceptibility device artifacts compared CMR. However, CCT typically affected by lower contrast‐to‐noise ratio potentially increased radiation exposure. Therefore, deep understanding available technology strategies acquisition optimization importance improve image quality accuracy, while minimizing This review summarizes principles on CCT, protocols according different technologies including dual‐energy innovative photon‐counting detector CT, setting clinical utility.

Language: Английский

Citations

0
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

et al.

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

Published: March 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.

Language: Английский

Citations

0
Comprehensive macro and micro views on immune cells in ischemic heart disease DOI Creative Commons
Yongjian Zhao, Mingyue Tan,

Yunfei Yin

et al.

Cell Proliferation, Journal Year: 2024, Volume and Issue: 57(12)

Published: Aug. 1, 2024

Ischemic heart disease (IHD) is a prevalent cardiovascular condition that remains the primary cause of death due to its adverse ventricular remodelling and pathological changes in end-stage failure. As complex pathologic condition, it involves intricate regulatory processes at cellular molecular levels. The immune system are closely interconnected, with cells playing crucial role maintaining cardiac health influencing progression. Consequently, alterations microenvironment influenced controlled by various cells, such as macrophages, neutrophils, dendritic eosinophils, T-lymphocytes, along cytokines they produce. Furthermore, studies have revealed Gata6

Language: Английский

Citations

3