Regulated Cell death in Acute Myocardial Infarction: Molecular Mechanisms and Therapeutic Implications

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 104, P. 102629 - 102629

Published: Dec. 5, 2024

Language: Английский

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Targeting FDX1 by trilobatin to inhibit cuproptosis in doxorubicin‐induced cardiotoxicity

British Journal of Pharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 11, 2025

Abstract Background and Purpose Doxorubicin (DOX), an anthracycline chemotherapeutic agent, whose use is limited owing to its dose‐dependent cardiotoxicity. Mitochondrial oxidative stress plays a crucial role in the pathogenesis of DOX‐induced cardiotoxicity (DIC). Trilobatin (TLB), naturally occurring food additive, exhibits strong antioxidant properties, but cardioprotective effects DIC unclear. This study investigates effect TLB on DIC. Experimental Approach DOX was used generate vivo vitro model Echocardiography, enzyme‐linked immunosorbent assay (ELISA) haematoxylin eosin (H&E) staining were evaluate cardiac function these models. To identify targets TLB, RNA‐sequence analysis, molecular dynamics simulations, surface plasmon resonance binding assays protein immunoblotting techniques used. Transmission electron microscopy, along with dihydroethidium Mito‐SOX staining, conducted examine impact trilobatin mitochondrial stress. SiRNA transfection performed confirm ferredoxin 1 (FDX1) development. Key Results In mice, improved manner inhibited myocardial fibrosis mice. also attenuated dysfunction reduced found directly bind FDX1 suppresses cuproptosis after treatment, causing significant inhibition cuproptosis‐related proteins. Conclusions Implications first show that strongly inhibits by reducing controlling DOX‐mediated targeting FDX1. Therefore, as potential phytochemical candidate for ameliorating

Language: Английский

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Panoptosis Targets the Mechanism of PRDX1 Involvement in Acute Myocardial Infarction via ZBP1

Journal of Cellular Biochemistry, Journal Year: 2025, Volume and Issue: 126(3)

Published: March 1, 2025

PANoptosis is involved in various pathological processes, but its role acute myocardial infarction (AMI) remains unclear. This study aimed to explore the mechanism by which AMI. GSE172270 was used as an internal test set, and GSE159657 served external validation set identify disease targets for WGCNA performed potential hub genes associated with Then, related among of AMI were screened. Additionally, human cardiomyocytes AC16 mouse HL-1 cultured sugar-free serum-free medium 4 h 12 h, expression key regulating detected qRT-PCR. Finally, mRNA interference overexpression experiments conducted verify mRNAs. A total 45 upregulated 125 downregulated differentially expressed (DEGs) identified data set. 891 In 695 552 DEGs identified. Four AMI-PANoptosis (PRDX1, MMACHC, BLVRB, TXNL1) Through qRT-PCR verification, PRDX1 most specific significant gene. The positive regulator ZPB1 upregulated, while negative TAK1 downregulated. cell death (MLKL, p-MLKL, Caspase-3, Caspase-7, GSDMD) culture. However, reversed these effects. Our demonstrated that a

Language: Английский

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PANoptosis: a potential target of atherosclerotic cardiovascular disease

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

Published: April 26, 2025

PANoptosis is a newly discovered cell death pathway triggered by the innate immunizer, which in turn promotes assembly of PANoptosome and activates downstream effectors. As special mode, it characterized apoptosis, pyroptosis, necroptosis at same time; therefore, not feasible to inhibit suppressing single pathway. However, active ingredients targeting can effectively PANoptosis.Given importance disease, would be an important therapeutic tool. Previous studies have focused more on infectious diseases cancer, role cardiovascular field has been comprehensively addressed. While ASCVD number one killer diseases, explore new targets determine future research directions. Therefore, this review focuses PANoptosome, molecular mechanism PANoptosis, related mechanisms leading such as myocardial infarction, ischemic cardiomyopathy stroke, order provide perspective for prevention treatment ASCVD.

Language: Английский

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Modulation of NLRP3 Inflammasome: Advantages of Chinese Herbal Medicine in Treating Myocardial Ischemia/Reperfusion Injury

The American Journal of Chinese Medicine, Journal Year: 2025, Volume and Issue: 53(03), P. 737 - 769

Published: Jan. 1, 2025

Myocardial ischemia/reperfusion (I/R) injury is characterized by severe inflammation and oxidative stress, involves the recruitment activation of immune cells, release pro-inflammatory cytokines, generation reactive oxygen species (ROS). The NOD-like receptor protein 3 (NLRP3) inflammasome, a multiprotein complex, activated when exposed to different danger signals like excessive ROS, changes in ionic flux, mitochondrial dysfunction. Once NLRP3 inflammasome activated, it promotes maturation cytokines such as interleukin-1β interleukin-18, which contributes inflammatory storm myocardial I/R injury. This cascade not only leads adverse cardiac remodeling but also impairs function, ultimately exacerbating clinical outcomes infarction. Despite critical role injury, there significant absence effective therapeutic strategies address practice. In recent years, Chinese herbal medicine has emerged promising candidate landscape exerts its cardioprotective effects through various mechanisms inhibiting inflammasomes, including enhancing reducing ROS generation, suppressing pyroptosis. review emphasizes potential extracts inhibit inflammasomes an effort develop treatments for It likewise summarizes research results interventions mechanism regulating providing insights development

Language: Английский

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The Potential Therapeutic Prospect of PANoptosis in Heart Failure

Journal of Inflammation Research, Journal Year: 2024, Volume and Issue: Volume 17, P. 9147 - 9168

Published: Nov. 1, 2024

Heart failure (HF) represents a serious manifestation or advanced stage of various cardiac diseases. HF continues to impose significant global disease burden, characterized by high rates hospitalization and fatality. Furthermore, the pathogenesis pathophysiological processes underlying remain incompletely understood, complicating its prevention treatment strategies. One mechanism associated with is systemic inflammatory response. PANoptosis, novel mode cell death, has been extensively studied in context infectious diseases, neurodegenerative disorders, cancers, other conditions. Recent investigations have revealed that PANoptosis-related genes are markedly dysregulated specimens. Consequently, PANoptosis-mediated response may represent potential therapeutic target for HF. This paper conducts comprehensive analysis molecular pathways drive PANoptosis. We discuss role targets HF, thereby providing valuable insights clinical development therapies.

Language: Английский

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