Peptide amphiphiles alleviate myocardial endoplasmic reticulum stress to enhance cardiomyocyte–macrophage communication and promote macrophage M2 polarization DOI
Wenjie Guo,

Hui-Ming Chen,

Fengjiao Liu

et al.

Journal of Controlled Release, Journal Year: 2024, Volume and Issue: 378, P. 719 - 734

Published: Dec. 28, 2024

Language: Английский

Cooling the Heart DOI Open Access
S. Tanveer Rab

Catheterization and Cardiovascular Interventions, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 12, 2025

Myocardial salvage remains the primary goal for aborting an episode of acute myocardial infarction. Rapid revascularization through PCI cornerstone therapy but may come at a cost reperfusion injury and further [1]. In this issue, Amario et al. [2] provide important metanalysis on cooling with mild therapeutic hypothermia (TH), before restoring coronary flow. While cooling, to reduce metabolic demands would make conceptual sense 10% decrease in infarct size (IS) every 1°C temperature experimental models, is result multiple factors that include reactive oxygen species, inflammation, calcium overload, endothelial dysfunction, impaired microvascular flow The authors included 10 RCT's their meta-analysis. Patients cardiac arrest receiving TH were excluded. concluded there was no benefit all cause death, IS, Thrombolysis Infarction (TIMI) blood flow, obstruction, ST segment resolution ECG, left ventricular ejection fraction, regardless induced by intracoronary or extra techniques matched population subsets. Adverse effects were, however, seen including increased risk infection, stent thrombosis, (in patients ischemic time < 4 h) atrial fibrillation, prolongation door balloon trend toward bleeding. Cardiologists are more commonly involved care resuscitated comatose postcardiac where used [3-6]. appears be reducing anoxic brain injury, heterogeneity reporting adverse as reported metanalysis. Of particular concern thrombosis after STEMI absorption antiplatelet drugs [7]. A shift from targeted management (TTM) normothermia prevention fever occurred TTM-2 HACA-ICA trials [5, 8] recent Class I guideline recommendation [9, 10]. With less arrythmias TTM 2 trial pneumonias trial. balance evidence events suggest cannot recommended routine not option patient. author declares conflicts interest.

Language: Английский

Citations

0

Peroxisome proliferator-activated receptor gamma (PPARG)-mediated myocardial salvage in acute myocardial infarction managed with left ventricular unloading and coronary reperfusion DOI Open Access
Joseph R. Visker, Eleni Tseliou, Christos P. Kyriakopoulos

et al.

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

Published: Feb. 15, 2025

Ischemic heart disease and acute myocardial infarction (AMI) is a leading cause of morbidity mortality. Improvements have been made in coronary interventions to restore blood flow, but ischemia/reperfusion (I/R) injury significantly impacts clinical outcomes. We previously reported that activation percutaneous mechanical unloading the left ventricle (LV) with transvalvular axial-flow device simultaneously reperfusion improves salvage. However, underlying mechanisms, potential adjuvant pharmacological timing use LV as cardioprotective approach AMI are not well understood. This study investigated a) mechanisms associated improved salvage, b) intervention, c) unloading. Following 90 minutes ischemia, adult swine were subjected alone, simultaneous reperfusion, upfront delayed unloading, or concurrent esmolol milrinone. Compared controls, group had 47% increase salvage following AMI. was increased expression neutrophil degranulation, macrophage activation, iNOS signaling, wound healing, PPAR signaling. From these pathways, PPARG (peroxisome proliferator-activated receptor gamma) emerged gene uniquely overexpressed unloaded reperfused myocardium. Next, we showed agonism rosiglitazone reduces mitochondrial oxygen demand cardiomyocytes vivo, I/R C57BL6/J mice. Thiazolidinediones (TZDs), such could be therapies combined mitigate injury.

Language: Английский

Citations

0

Cardioprotective potential of transcription factor PRRX1 silencing against myocardial ischemia/reperfusion injury by regulating excessive mitophagy and ferroptosis through FKBP5-p38 MAPK axis DOI

Yongpeng Fang,

Xudong Niu,

Weifang Zhao

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2025, Volume and Issue: 1871(5), P. 167766 - 167766

Published: March 3, 2025

Language: Английский

Citations

0

Association of Intramyocardial Hemorrhage With Inflammatory Biomarkers in Patients With ST-Segment Elevation Myocardial Infarction DOI Creative Commons

Christina Tiller,

Martin Reindl, Magdalena Holzknecht

et al.

JACC Advances, Journal Year: 2025, Volume and Issue: 4(4), P. 101647 - 101647

Published: March 12, 2025

Language: Английский

Citations

0

Macrophage and cardiomyocyte roles in cardioprotection: Exploiting the NLRP3 Inflammasome inhibitor INF150 DOI Creative Commons
Magalì Giordano, Saveria Femminò, Federica Blua

et al.

Vascular Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 107487 - 107487

Published: March 1, 2025

Language: Английский

Citations

0

Necroptosis in myocardial ischaemia-reperfusion injury: current update on mechanisms, therapeutic targets, and translational potential DOI
Siarhei A. Dabravolski, Vladislav Kalmykov,

Anastasia O Maksaeva

et al.

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

Published: March 27, 2025

Language: Английский

Citations

0

Autophagy: a double-edged sword in ischemia–reperfusion injury DOI Creative Commons
Laura H. Tang,

Wangzheqi Zhang,

Liao Yan

et al.

Cellular & Molecular Biology Letters, Journal Year: 2025, Volume and Issue: 30(1)

Published: April 7, 2025

Abstract Ischemia–reperfusion (I/R) injury describes the pathological process wherein tissue damage, initially caused by insufficient blood supply (ischemia), is exacerbated upon restoration of flow (reperfusion). This phenomenon can lead to irreversible damage and commonly observed in contexts such as cardiac surgery stroke, where temporarily obstructed. During ischemic conditions, anaerobic metabolism tissues organs results compromised enzyme activity. Subsequent reperfusion exacerbates mitochondrial dysfunction, leading increased oxidative stress accumulation reactive oxygen species (ROS). cascade ultimately triggers cell death through mechanisms autophagy mitophagy. Autophagy constitutes a crucial catabolic mechanism within eukaryotic cells, facilitating degradation recycling damaged, aged, or superfluous organelles proteins via lysosomal pathway. essential for maintaining cellular homeostasis adapting diverse conditions. As self-degradation clearance mechanism, exhibits dualistic function: it confer protection during initial phases injury, yet potentially exacerbate later stages. paper aims elucidate fundamental I/R highlighting its dual role regulation effects on both organ-specific systemic responses. By comprehending their implications organ function, this study seeks explore potential therapeutic interventions modulation clinical settings.

Language: Английский

Citations

0

Cardiosplenic axis-targeted immunomodulatory liposome for myocardial ischemia-reperfusion injury treatment DOI
Jing Dong, Zechuan Li,

Chenxing Fu

et al.

Journal of Controlled Release, Journal Year: 2025, Volume and Issue: 383, P. 113799 - 113799

Published: May 3, 2025

Language: Английский

Citations

0

Immune in myocardial ischemia/reperfusion injury: potential mechanisms and therapeutic strategies DOI Creative Commons

Xiaoyu Xuan,

Jilin Fan, Jingyi Zhang

et al.

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

Published: May 8, 2025

Myocardial infarction (MI), which is characterized by high morbidity and mortality, a serious threat to human life health, timely reperfusion therapy save ischemic myocardium currently the most effective intervention. Although effectively restores coronary blood flow maximally limits infarct size, it triggers additional cell death tissue damage, known as myocardial ischemia/reperfusion injury (MIRI). Multiple immune cells are present in area, executing specific functions engaging crosstalk during diverse stages, constituting complex microenvironment involved repair regeneration after MIRI. Immunotherapy brings new hope for treating heart disease modulating microenvironment. In this paper, we explore regulatory roles of various MIRI close relationship between different deaths addition, current status research on targeting system intervene MIRI, with expectation providing basis achieving clinical translation.

Language: Английский

Citations

0

Acupuncture attenuates myocardial ischemia/reperfusion injury-induced ferroptosis via the Nrf2/HO-1 pathway DOI Creative Commons
Xiao Li, Yuxin Sun, Adi Wirawan Tjahjono

et al.

Chinese Medicine, Journal Year: 2025, Volume and Issue: 20(1)

Published: May 9, 2025

Abstract Aims To observe the effect of electro-acupuncture (EA) on cardiomyocytes ferroptosis induced by myocardial ischemia/reperfusion injury (MIRI) in mice and to investigate whether this occurs via nuclear factor-E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) signalling pathway. Materials methods Firstly, Fe 2+ hearts serum from both sham-operated (SO) group MIRI was measured ascertain had occurred group. In second phase, EA administered, with sham acupuncture (SA) as comparator, protective effects cardiac function. Additionally, we studied levels Nrf2 HO-1 within myocardium. third inhibitor ML385 agonist DMF were applied impact inhibiting therapeutic efficacy EA. Results Compared SO group, showed increased iron deposition, along a significant decrease levels. + exhibited significantly improved function reduced accompanied Furthermore, superior that SA Administration partially blocked anti-ferroptotic cardioprotective EA, while treatment similar dimethyl fumarate (DMF) intervention. Conclusion alleviates ferroptosis-induced damage Nrf2/HO-1 pathway, providing modern scientific evidence for application cardiovascular diseases.

Language: Английский

Citations

0