Identification of biomarkers of renal ischemia-reperfusion injury by bioinformatics analysis and single-cell sequencing analysis combined with in vivo validation DOI Creative Commons
Qin Zhu,

Shiqi Ren,

Zhaoyang Sun

и другие.

Transplant Immunology, Год журнала: 2023, Номер 81, С. 101928 - 101928

Опубликована: Сен. 11, 2023

Renal ischemia-reperfusion injury (IRI) is a serious clinical complication of kidney injury. This research dealt with investigating the hub genes and pathways associated renal IRI.

Язык: Английский

The emerging role of regulated cell death in ischemia and reperfusion-induced acute kidney injury: current evidence and future perspectives DOI Creative Commons

Chenning Li,

Ying Yu, Shuainan Zhu

и другие.

Cell Death Discovery, Год журнала: 2024, Номер 10(1)

Опубликована: Май 4, 2024

Abstract Renal ischemia‒reperfusion injury (IRI) is one of the main causes acute kidney (AKI), which a potentially life-threatening condition with high mortality rate. IRI complex process involving multiple underlying mechanisms and pathways cell dysfunction. Additionally, various types death have been linked to IRI, including necroptosis, apoptosis, pyroptosis, ferroptosis. These processes operate differently varying degrees in different patients, but each plays role pathological conditions AKI. Advances understanding pathophysiology will lead development new therapeutic approaches that hold promise for improving outcomes patients This review provides an overview recent research on molecular IRI-AKI, focus regulated (RCD) forms such as Overall, targeting RCD shows potential approach treating IRI-AKI.

Язык: Английский

Процитировано

13

Different types of cell death and their interactions in myocardial ischemia–reperfusion injury DOI Creative Commons

Bingxin Du,

Qiang Fu, Qin Yang

и другие.

Cell Death Discovery, Год журнала: 2025, Номер 11(1)

Опубликована: Март 5, 2025

Myocardial ischemia-reperfusion (I/R) injury is a multifaceted process observed in patients with coronary artery disease when blood flow restored to the heart tissue following ischemia-induced damage. Cardiomyocyte cell death, particularly through apoptosis, necroptosis, autophagy, pyroptosis, and ferroptosis, pivotal myocardial I/R injury. Preventing death during of vital for improving ischemic cardiomyopathy. These multiple forms can occur simultaneously, interact each other, contribute complexity In this review, we aim provide comprehensive summary key molecular mechanisms regulatory patterns involved these five types We will also discuss crosstalk intricate interactions among mechanisms, highlighting interplay between different death. Furthermore, explore specific molecules or targets that participate pathways elucidate their action. It important note manipulating distinct processes may have significant impact on reducing By enhancing researchers' understanding injury, review aims pave way development novel interventions cardio-protection affected by

Язык: Английский

Процитировано

1

Tumor Necrosis Factor Family Members and Myocardial Ischemia-Reperfusion Injury: State of the Art and Therapeutic Implications DOI Open Access
Antonella Galeone, Maria Grano, Giacomina Brunetti

и другие.

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(5), С. 4606 - 4606

Опубликована: Фев. 27, 2023

Ischemic heart disease is the principal cause of death worldwide and clinically manifests as myocardial infarction (MI), stable angina, ischemic cardiomyopathy. Myocardial defined an irreversible injury due to severe prolonged ischemia inducing cell death. Revascularization helpful in reducing loss contractile myocardium improving clinical outcome. Reperfusion rescues from but also induces additional called ischemia-reperfusion injury. Multiple mechanisms are involved injury, such oxidative stress, intracellular calcium overload, apoptosis, necroptosis, pyroptosis, inflammation. Various members tumor necrosis factor family play a key role In this article, TNFα, CD95L/CD95, TRAIL, RANK/RANKL/OPG axis regulation tissue damage reviewed together with their potential use therapeutic target.

Язык: Английский

Процитировано

21

Connexin32 gap junction channels deliver miR155-3p to mediate pyroptosis in renal ischemia-reperfusion injury DOI Creative Commons

Liubing Chen,

Hongyi Fang,

Xiaoyun Li

и другие.

Cell Communication and Signaling, Год журнала: 2024, Номер 22(1)

Опубликована: Фев. 12, 2024

Abstract Objectives To explore whether the gap junction (GJ) composed by connexin32(Cx32) mediated pyroptosis in renal ischemia-reperfusion(I/R) injury via transmitting miR155-3p, with aim to provide new strategies for prevention and treatment of acute kidney (AKI) after I/R. Methods 8–10 weeks male C57BL/ 6 wild-type mice Cx32 knockdown were divided into two groups respectively: control group I/R group. MCC950 (50 mg/kg. ip.) was used inhibit NLRP3 vivo. Human tubular epithelial cells (HK - 2) rat (NRK-52E) high-density low-density group, treated hypoxia reoxygenation (H/R) mimic The siRNA plasmid Cx32, inhibitor miR155-3p transfected HK 2 respectively. Kidney pathological functional injuries measured. Western Blot immunofluorescent staining observe expression NLRP3, GSDMD, GSDMD-N, IL 18, mature IL-18. secretion IL-18 IL-1β serum, tissue supernatant detected enzyme-linked immuno sorbent assay (ELISA) kit, NLPR3 RT-qPCR fluorescence situ hybridization (FISH). Results Tubular found promote AKI vivo Cx32-GJ regulated affecting injury. In vitro, H/R could lead HK-2 NRK-52E cells. When GJ channels not formed, inhibited or knockdown, significantly reduced obviously inhibited, leading reduction increase survival rate. Moreover, regulating level affect rate vitro H/R. Conclusions miR155-3p. Inhibition reduce further pyroptosis, alleviation which provided a strategy preventing occurrence AKI.

Язык: Английский

Процитировано

6

Research progress on the mechanism of curcumin in cerebral ischemia/reperfusion injury: a narrative review DOI
Liyuan Zhang, Yibo Han, Xuelan Wu

и другие.

APOPTOSIS, Год журнала: 2023, Номер 28(9-10), С. 1285 - 1303

Опубликована: Июнь 26, 2023

Язык: Английский

Процитировано

15

Taohong Siwu decoction reduces acute myocardial ischemia–reperfusion injury by promoting autophagy to inhibit pyroptosis DOI Creative Commons
Yuming Yang, Ying Zhu, Changyi Liu

и другие.

Journal of Ethnopharmacology, Год журнала: 2023, Номер 321, С. 117515 - 117515

Опубликована: Ноя. 30, 2023

Taohong Siwu decoction (TSD) is a classic traditional Chinese medicine (TCM) prescription used to promote the blood circulation and alleviate stasis. TSD consists of Paeonia lactiflora Pall., Conioselinum anthriscoides (H. Boissieu) Pimenov & Kljuykov, Rehmannia glutinosa (Gaertn.) DC., Prunus persica (L.) Batsch, Angelica sinensis (Oliv.) Diels, Carthamus creticus L. in ratio 3:2:4:3:3:2. Studies on effects myocardial ischemia-reperfusion injury (MIRI) from perspective autophagy pyroptosis have not been reported.

Язык: Английский

Процитировано

13

Identification and validation of mitochondrial dynamics-related genes in patients with acute myocardial infarction-a bioinformatics analysis DOI Creative Commons

Xiaolin Yue,

Jinlei Wu,

Xue-yun Shi

и другие.

Research Square (Research Square), Год журнала: 2025, Номер unknown

Опубликована: Янв. 2, 2025

Abstract Recent studies highlight the link between cardiovascular disease and mitochondrial dynamics. This study sought biomarkers of dynamics in acute myocardial infarction (AMI) to guide more precise clinical management. AMI-related datasets (GSE62646 GSE59867) 50 dynamics-related genes (MD-RGs) were derived from public databases. Firstly, based on MD-RGs, AMI samples GSE62646 classified into high- low-scoring groups by single-sample gene set enrichment analysis. The differentially expressed (DEGs) incorporated machine learning algorithms. Subsequent expression level receiver operating characteristic (ROC) analyses identified biomarkers. Furthermore, relationship was analyzed analysis, immune infiltration correlation analysis m6A regulators. Finally, biomarker verified reverse transcription quantitative PCR (RT-qPCR). In this study, COX7B SNORD54 as associated with AMI. ROC curves showed that two could better differentiate control samples, subsequent nomogram created integrating highly accurate predicting revealed co-enrich pathways for included “oxidative phosphorylation” “Notch signaling pathway”. Notably, six regulators (HNRNPC, KIAA1429, METTL3, WTAP, YTHDC1, YTHDC2) found be significantly under-expressed samples. RT-PCR demonstrated levels downregulated compared controls. recognized AMI, presenting potential applications advance understanding

Язык: Английский

Процитировано

0

Identifying Pyroptosis-Hub Genes and Inflammation Cell Type-Related Genes in Ischemic Stroke DOI Creative Commons

Wei Ge,

Liangbin Cao,

Can Liu

и другие.

Molecular Neurobiology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 3, 2025

Stroke is the second-leading global cause of death. The damage attributed to immune storm triggered by ischemia–reperfusion injury (IRI) post-stroke substantial. However, data on transcriptomic dynamics pyroptosis in IRI are limited. This study aimed analyze expression key genes stroke and their correlation with infiltration. Pyroptosis-related were identified from obtained middle cerebral artery occlusion (MCAO) datasets. Differential functional analyses pyroptosis-related performed, differences enrichment between high-risk low-risk groups determined. An MCAO diagnostic model was constructed validated using selected differential expression. High- for cell analysis hub genes. A regulatory network miRNA also constructed, protein domains predicted. an rat model. Twenty-five showed expression, including four genes, namely WISP2, MELK, SDF2L1, AURKB. Characteristic verified real-time quantitative PCR analyses. high- significant SDF2L1. In infiltration analysis, 12 cells samples. Further demonstrated positive correlations gene SDF2L1 cell-activated dendritic group natural killer group. elevated closely associated inflammatory types can predict ischemic risk levels help facilitate treatment.

Язык: Английский

Процитировано

0

Effects of Ellagic Acid and Berberine on Hind Limb Ischemia Reperfusion Injury: Pathways of Apoptosis, Pyroptosis, and Oxidative Stress DOI Creative Commons
Esra Tekin, Ali Koray Kaya, Ays̀egül Küçük

и другие.

Medicina, Год журнала: 2025, Номер 61(3), С. 451 - 451

Опубликована: Март 4, 2025

Background and Objectives: Hind limb ischemia–reperfusion (I/R) injury is a serious clinical condition that requires urgent treatment develops as result of sudden decrease in blood flow the extremity. Antioxidant combinations are frequently used diseases today. This study aimed to investigate compare effectiveness ellagic acid (EA) berberine (BER), which important antioxidants, combination on hind I/R evaluate their therapeutic power. Materials Methods: Thirty-five male Sprague Dawley rats were randomly divided into five groups: sham, I/R, EA+I/R, BER+I/R, EA/BER+I/R. In procedure, infrarenal abdominal aorta was clamped reperfused for 2 h. EA (100 mg/kg, ip) BER (200 administered 75th minute ischemia. Oxidative stress markers (MDA, GSH, SOD, CAT) TNF-α measured. Apoptosis (Bax, Bcl-2, Cleaved caspase-3) pyroptosis (Nrf2, NLRP3, Gasdermin D) pathways evaluated via Western blot. Muscle tissue examined histopathologically by hematoxylin eosin staining. One-way ANOVA post hoc LSD tests applied statistical analyses (p < 0.05). Results: Bax levels increased ischemia group decreased with Bcl-2 but The highest level Bax/Bcl-2 ratio caspase 3 higher other groups compared sham While Nrf2 group, NLRP3 D increased; normalized these histopathological analysis, reduced damage similar between > MDA BER, CAT Conclusions: It concluded depend degree duration inflammation no difference found relation this study. As result, EA, could be potential agents positive effects.

Язык: Английский

Процитировано

0

Ischemia-reperfusion injury induces ZBP1-dependent PANoptosis in endothelial cells DOI
Yue Cui,

Lin Huang,

Jiaxing Ma

и другие.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Год журнала: 2025, Номер unknown, С. 167782 - 167782

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0