Ferroptosis Genes and ST-segment Elevation Myocardial Infarction Outcomes: A Predictive Signature DOI Creative Commons
Xingjie Wang, Lei Huang, Min Hou

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 11(1), P. e41534 - e41534

Published: Dec. 27, 2024

The aim of this paper is to discover differentially expressed genes related ferroptosis (DEFRGs) in patients with ST-segment elevation myocardial infarction (STEMI) and construct a reliable prognostic signature that incorporates key DEFRGs easily accessible clinical factors. We did systematic review Gene Expression Omnibus datasets picked SE49925, GSE60993, GSE61144 for analysis. applied GEO2R find overlapped them among the datasets. performed functional enrichment analysis explore their biological functions. built an optimal model least absolute shrinkage selection operator (LASSO) penalized Cox proportional hazards regression. tested value survival analysis, ROC curve, decision curve nomogram. also confirmed externally plasma samples from our center's patients. A combining three overexpressed (ACSL1, ACSL4, TSC22D3) two variables (serum creatinine level, Gensini score) was established. effectively classified into low- high-risk groups. Survival DCA showed its robust predictive performance utility within years after onset disease. external validation cohort significant difference major adverse cardiovascular events (MACEs) between This study revealed STEMI developed integrates gene expression levels factors stratifying predicting risk MACEs.

Language: Английский

Endoplasmic reticulum stress-mediated cell death in cardiovascular disease DOI Creative Commons

Yajuan An,

Xinshuang Wang,

Xiuju Guan

et al.

Cell Stress and Chaperones, Journal Year: 2024, Volume and Issue: 29(1), P. 158 - 174

Published: Jan. 29, 2024

The endoplasmic reticulum (ER) plays a vital function in maintaining cellular homeostasis. Endoplasmic stress (ERS) can trigger various modes of cell death by activating the unfolded protein response (UPR) signaling pathway. Cell crucial role occurrence and development diseases such as cancer, liver diseases, neurological cardiovascular diseases. Several including hypertension, atherosclerosis, heart failure are associated with ER stress. stress-mediated is interest disease. Moreover, an increasing body evidence supports potential modulating ERS for treating This paper provides comprehensive review UPR pathway, mechanisms that induce death, Additionally, we discuss common along therapeutic strategies.

Language: Английский

Citations

15
Metrnl and Cardiomyopathies: From Molecular Mechanisms to Therapeutic Insights DOI Creative Commons

Miaomiao Xu,

Xiaoguang Liu, Liming Lu

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2025, Volume and Issue: 29(2)

Published: Jan. 1, 2025

ABSTRACT Cardiomyopathies, a diverse group of diseases affecting the heart muscle, continue to pose significant clinical challenges due their complex aetiologies and limited treatment options targeting underlying genetic molecular dysregulations. Emerging evidence indicates that Metrnl, myokine, adipokine cardiokine, plays role in pathogenesis various cardiomyopathies. Therefore, objective this review is examine mechanism Metrnl cardiomyopathies, with expectation providing new insights for these diseases.

Language: Английский

Citations

1
Targeting Zfp36 to combat cardiac hypertrophy: Insights into ferroptosis pathways DOI Creative Commons
Mingyu Zhang, Xiaoxiang Guan, Zheng Dong

et al.

Clinical and Translational Medicine, Journal Year: 2025, Volume and Issue: 15(3)

Published: Feb. 25, 2025

Cardiac hypertrophy is a precursor to heart failure and represents significant global cause of mortality, thereby necessitating timely effective therapeutic interventions. Zinc finger protein 36 (Zfp36) recognised as critical regulator ferroptosis; however, its role underlying mechanisms in cardiac remain largely unexplored. This study aims investigate the regulatory function Zfp36 ferroptosis within context hypertrophy. Single-cell sequencing analysis demonstrated reduction expression associated with was observed mitigate reduce hypertrophic phenotypes cardiomyocytes subjected Angiotensin II (Ang II) myocardial tissues induced by transverse aortic constriction. The inhibitor Ferrostatin-1 shown alleviate when co-incubated si-Zfp36 Ang II. Mechanistically, binds 3' untranslated region (3'UTR) Ythdc2 mRNA, facilitating degradation. subsequently SLC7A11 enhancing decay, which leads glutathione (GSH) levels, exacerbating Furthermore, overexpression reversed protective effects conferred Zfp36, while silencing counteracted knockdown. elucidates hypertrophy, specifically detailing modulatory mechanism via Ythdc2/SLC7A11/GSH pathway. These insights lay groundwork for innovative approaches understanding pathological clinical initially attenuate through inhibition cardiomyocytes, providing new target strategies targeting ferroptosis. facilitated degradation mRNA binding it, inhibiting Ythdc2-mediated maintaining GSH levels. previously unrecognized pathway

Language: Английский

Citations

1
The Role of Cdo1 in Ferroptosis and Apoptosis in Cancer DOI Creative Commons
Xiaoyi Chen, Ansgar Poetsch

Biomedicines, Journal Year: 2024, Volume and Issue: 12(4), P. 918 - 918

Published: April 20, 2024

Cysteine dioxygenase type 1 (Cdo1) is a tumor suppressor gene. It regulates the metabolism of cysteine, thereby influencing cellular antioxidative capacity. This function puts Cdo1 in prominent position to promote ferroptosis and apoptosis. promotes mainly by decreasing amounts antioxidants, leading autoperoxidation cell membrane through Fenton reaction. apoptosis product cysteine metabolism, taurine, low level antioxidants. Many cancers exhibit altered Cdo1, underscoring its crucial role cancer survival. Genetic epigenetic alterations have been found, with methylation promoter as most common mutation. The fact that no was found be caused alone indicates mild. By compiling current knowledge about apoptosis, ferroptosis, this review suggests possibilities for how mild anticancer could harnessed new therapies. Here, developing drugs targeting considered meaningful neoadjuvant therapies, example, helping against development anti-cancer drug resistance cells.

Language: Английский

Citations

4
NDRG1 regulates iron metabolism and inhibits pathological cardiac hypertrophy DOI
Jiali Yuan,

Chengye Yin,

Hong Peng

et al.

Canadian Journal of Cardiology, Journal Year: 2024, Volume and Issue: 41(2), P. 224 - 240

Published: Oct. 18, 2024

Language: Английский

Citations

4
Transcriptome Insights into Protective Mechanisms of Ferroptosis Inhibition in Aortic Dissection DOI Creative Commons

Chun-Che Shih,

Chi‐Yu Chen, Chih‐Pin Chuu

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 21, 2025

Abstract Aortic dissection (AD) is a life-threatening vascular condition with limited pharmacological options. This study investigated Ferrostatin-1 (Fer-1), ferroptosis inhibitor, in BAPN/Ang-II-induced mouse model of AD, revealing significant therapeutic potential. Fer-1 significantly reduced AD incidence and mortality by preserving aortic wall integrity. RNA sequencing identified 922 differentially expressed genes, 416 upregulated 506 downregulated. Bioinformatics analysis revealed that modulates key regulators, such as MEF2C KDM5A, impacting immune responses, oxidative stress, apoptosis, lipid metabolism. Additionally, alters miRNA expression, the upregulation miR-361-5p downregulation miR-3151-5p, targeting pathways involved inflammation, smooth muscle cell (SMC) phenotypic stability. Functional pathway highlighted inhibition actin cytoskeleton, ILK, IL-17 signaling, essential for SMC differentiation extracellular matrix remodeling. Gene interaction network 21 central molecules, including CXCR3, ACACA, BPGM, associated metabolism, These findings demonstrate Fer-1's potential to mitigate modulate offering comprehensive protective mechanism against potentially other ferroptosis-driven diseases.

Language: Английский

Citations

0
Semaglutide attenuates myocardial ischemia-reperfusion injury by inhibiting ferroptosis of cardiomyocytes via activation of PKC-S100A9 axis DOI Creative Commons
Yan Liu, Zixuan Li, Xiaomeng Xu

et al.

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

Published: March 20, 2025

Objective The incidence of ischemic cardiomyopathy increases annually worldwide, and it is the leading cause mortality in China. Although interventional diagnostic therapeutic techniques can promptly open culprit vessels, myocardial ischemia-reperfusion injury (MIRI), resulting from restored blood flow, often inevitable. Semaglutide (Sem), a novel GLP-1 analogue, primarily utilized managing Type 2 diabetes mellitus (T2DM). Recent research indicates that semaglutide may reduce risk major adverse cardiovascular events. Therefore, purpose this study to explore whether ameliorate MIRI its potential mechanism. Methods results : A mouse model (I/R) was created by ligating left anterior descending coronary artery (LAD) first for 45 min then reperfusing heart 24 h. Assessment cardiac function fibrosis were conducted through small animal ultrasound Masson’s staining. It observed enhanced recovery diminished I/R model. In vivo experiments, proved mitigate oxidative stress inhibit ferroptosis cardiomyocytes. RNA sequencing showed S100 calcium binding protein A9 (S100A9) target gene protect against MIRI. vitro , experiments decreased expression S100A9 activating Protein Kinase C(PKC) pathway, thus inhibiting Conclusion I/R-induced mechanism, mainly via activation PKC signaling pathway. considered as treatment option

Language: Английский

Citations

0
Mitochondrial function: A new direction for the targeted treatment of cardiovascular diseases with Chinese herbal medicine DOI Creative Commons
Lin Yang, Liang Wang, Baofeng Yang

et al.

Journal of Holistic Integrative Pharmacy, Journal Year: 2025, Volume and Issue: 6(1), P. 91 - 104

Published: March 1, 2025

Language: Английский

Citations

0
Identification of hub genes for the diagnosis associated with heart failure using multiple cell death patterns DOI Creative Commons
Huajing Yuan, Hui Yu, Yiding Yu

et al.

ESC Heart Failure, Journal Year: 2025, Volume and Issue: unknown

Published: April 10, 2025

Abstract Aims Heart failure (HF) is an important public health problem worldwide, and programmed cell death (PCD) plays a crucial role in its pathologic process. This study aims to identify the hub genes associated with HF through PCD order better understand pathogenesis of improve diagnosis treatment. Methods results The gene expression dataset was obtained from GEO database. Bioinformatics machine learning algorithms were utilized screen key PCD‐related genes, diagnostic model constructed on this. Functional enrichment analysis clarified ontology signalling pathways HF. immune infiltration performed explore levels cells each gene. Through bioinformatics analysis, 95 obtained. showed that they mainly involved inflammation, immunomodulation other mechanisms. DHRS11 LRKK2 identified as PCD‐associated by algorithms. confirmed significant biomarkers training validation datasets, their nomogram had effective value. Immune imbalance T‐cell populations, monocytes macrophages M2 Conclusions In this study, genes. construction analyses performed, which provided new ideas for molecular mechanisms development

Language: Английский

Citations

0
Advances in Mechanisms of Ferroptosis in Cardiovascular Disease DOI

婷 李

Advances in Clinical Medicine, Journal Year: 2025, Volume and Issue: 15(04), P. 1433 - 1440

Published: Jan. 1, 2025

Language: Английский

Citations

0