Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Journal Year: 2023, Volume and Issue: 1870(6), P. 119480 - 119480
Published: April 30, 2023
Language: Английский
Journal of Cellular and Molecular Medicine, Journal Year: 2023, Volume and Issue: 27(20), P. 3075 - 3089
Published: July 24, 2023
Resveratrol is an organic compound widely studied for its therapeutic uses. We investigated whether resveratrol exerts cardioprotective effects by inhibiting ferroptosis via the Sirt1/p53 pathway. A heart failure model was established aortic coarctation in Sirt1 knockout mice. The superoxide dismutase (SOD), glutathione (GSH) levels and mitochondrial morphology murine tissues were assessed at different time points to determine role of progression. cardiac function mice with evaluated determining brain natriuretic peptide (BNP) sST2 concentration conducting echocardiography. Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) transfected p53 K382R mutant interference lentiviral vectors. Immunoprecipitation (IP) experiments performed investigate influences K382 acetylation SLC7A11 expression modulation. improved decelerated fibrosis progression failure. However, ability prevent treat lost after silencing Sirt1. reduced diminishing acetylation, reducing degradation SLC7A11, increasing GSH peroxidase 4 (GPX4) cells. In conclusion, activating pathway failure, decreased depletion inhibited ferroptosis, function.
Language: Английский
Citations
38
Clinical and Experimental Hypertension, Journal Year: 2023, Volume and Issue: 45(1)
Published: Feb. 13, 2023
As a common and frequently occurring disease, heart failure has been paid more attention, but the mechanism of its occurrence development is still unclear. This study investigated that PGAM5 expression levels in underlying mechanisms vivo vitro.The inhibition mRNA patients with was compared normal group.The serum negative correlation collagen I III failure. protein tissue mice were down-regulated at time-dependent rate. The presented model. reduced inflammation inhibited ROS-induced oxidative stress models Ferroptosis regulated Keap1/Nrf2 signaling pathway. IP also showed combined Keap1 protein. could increase ubiquitination. affected effects model failure.We conclude protection ferroptosis by pathway failure, suggesting targeting this may be feasible strategy to treat
Language: Английский
Citations
28
Frontiers in Endocrinology, Journal Year: 2023, Volume and Issue: 14
Published: April 20, 2023
Diabetic cardiomyopathy (DCM) is a serious complication of type 1 and 2 diabetes, which leads to the aggravation myocardial fibrosis, disorders involving systolic diastolic functions, increased mortality patients with diabetes through mechanisms such as glycolipid toxicity, inflammatory response, oxidative stress. Ferroptosis form iron-dependent regulatory cell death that attributed accumulation lipid peroxides an imbalance in redox regulation. Increased production reactive oxygen species (ROS) during ferroptosis promotes stress damages cells, leading dysfunction. Overproduction ROS important bridge between DCM, inhibitors may provide new targets for treatment DCM.
Language: Английский
Citations
27
Phytomedicine, Journal Year: 2024, Volume and Issue: unknown, P. 155357 - 155357
Published: Jan. 1, 2024
The terminal stage of all cardiovascular diseases typically culminates in heart failure (HF), with no effective intervention available to halt its progression. LuQi formula (LQF) has been employed clinical for numerous years significantly ameliorate cardiac function HF patients. Nevertheless, the underlying mechanism LQF's efficacy remains inadequately comprehended. Cardiomyocyte ferroptosis served as a pathogenic HF. goal current experiment was ascertain whether LQF ameliorates by preventing cardiomyocyte and elucidate intrinsic involved. This research objective is investigate impact attenuating failure. Transverse aortic constriction (TAC) performed construct mouse model. Neonatal rat cardiomyocytes (NRCMs) were subjected vitro experiments. High-performance liquid chromatography (HPLC) identified bioactive compounds LQF. Transcriptomic quantitative proteomic analyses revealed potential targets anti-HF. Specifically, histological staining evaluated hypertrophy fibrosis. Transmission electron microscopy (TEM) observed mitochondrial morphology. content Fe2+, ROS, MDA, GSH, GSSH detected using kits. Molecular docking binding activities between essential active ingredients critical proteins ferroptosis. Mechanistically, expression levels Nrf2, Keap1, HO-1, SLC7A11, GPX4 qPCR, Western blot (WB), or immunohistochemical staining. primary nine detected. demonstrated that may Histomorphometric attenuates myocardial TEM diminished shrinkage increased membrane density tissue. Additionally, reactive oxygen species (ROS) generation suppressed Furthermore, molecular technique had suitable GPX4, SLC7A11. analysis further verified activated Nrf2/GPX4 signaling axis. decreased SLC7A11 HO-1 expression. These results prevents via activating axis suppressing Concurrently, it contributed elucidating provided scientific rationale development novel therapeutic drug.
Language: Английский
Citations
12
The FASEB Journal, Journal Year: 2024, Volume and Issue: 38(2)
Published: Jan. 18, 2024
Abstract Ferroptosis, a type of iron‐catalyzed necrosis, is responsible for vascular smooth muscle cell (VSMC) death and serves as potential therapeutic target alleviating aortic aneurysm. Here, our study explored the underlying mechanism ferroptosis affecting VSMC functions resultant formation AAA using its inhibitor Ferrostatin‐1 (Fer‐1). Microarray‐based gene expression profiling was employed to identify differentially expressed genes related ferroptosis. An model established by angiotensin II (Ang II) induction in apolipoprotein E‐knockout (ApoE −/− ) mice, followed injection Fer‐1 RSL‐3 (ferroptosis inducer). Then, role VSMCs analyzed Ang II‐induced mice. Primary mouse were cultured vitro treated with II, Fer‐1, sh‐SLC7A11, or sh‐GPX4 assess effect via SLC7A11/GPX axis. Bioinformatics analysis revealed that GPX4 involved fibrosis AAA, there an interaction between SLC7A11 GPX4. In assays showed alleviated retard consequent formation. The associated activation SLC7A11/GPX4 pathway. Silencing could inhibit ameliorating on VSMCs. vivo animal studies further demonstrated inhibited vessel wall structural abnormalities through may prevent
Language: Английский
Citations
12
Analytical Chemistry, Journal Year: 2024, Volume and Issue: 96(5), P. 2041 - 2051
Published: Jan. 25, 2024
Ferroptosis is critical in the treatment of tumor therapies. Thus, monitoring reactive oxygen species (ROS) great significance for accurate assessment ferroptosis without any interference. However, current probes ROS during suffer from a drawback that consume detection, which inhibits process and thus affects accuracy effectiveness ferroptosis. Herein, new fluorescent donor probe, TFMU-SO2D, with combination moiety SO2 designed synthesized by introducing aryl boronate moieties could give it ability to effectively recognize ONOO–. The released excess glutathione regulate oxidative stress elevating levels, would offset depletion TFMU-SO2D ensure process. experimental results demonstrated possessed satisfactory performance ONOO– as well simultaneously releasing stimulated monensin erastin RSL3. Additionally, capability synergized inhibit viability cancer cells was CCK8 assay, may be due fact can potentiate cell death increasing level. Overall, these combined indicated possesses excellent precisely monitor interference, significant accurately accessing ferroptosis, treatment, drug development.
Language: Английский
Citations
12
International Journal of Medical Sciences, Journal Year: 2024, Volume and Issue: 21(4), P. 612 - 622
Published: Jan. 1, 2024
Diabetic cardiomyopathy (DC) is a pathophysiologic condition caused by diabetes mellitus (DM) in the absence of coronary artery disease, valvular heart and hypertension that can lead to failure (HF), manifesting itself early stages with left ventricular hypertrophy diastolic dysfunction, marked HF decreased systolic function later stages.There still lack direct evidence prove exact existence DC.Ferroptosis novel form cell death characterized reactive oxygen species (ROS) accumulation lipid peroxidation.Several animal studies have shown ferroptosis closely related DC progression.This review systematically summarizes pathogenic mechanisms DC, including reduction cardiac RDH10 induced cardiomyocytes which mediated retinol metabolism disorders; CD36 overexpression deposition GPX4 expression cardiomyocytes, leading development ferroptosis; Nrf2 iron overload peroxidation promoted lncRNA-ZFAS1 as ceRNA, combined miR-150-5p inhibit CCND2 thereby triggering ferroptosis.
Language: Английский
Citations
10
Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 174, P. 116457 - 116457
Published: March 22, 2024
Ferroptosis, distinct from apoptosis, necrosis, autophagy, and other types of cell death, is a novel iron-dependent regulated death characterized by the accumulation lipid peroxides redox imbalance with morphological, biochemical, genetic features. Dysregulation iron homeostasis, disruption antioxidative stress pathways peroxidation are crucial in ferroptosis. Ferroptosis involved pathogenesis several cardiovascular diseases, including atherosclerosis, cardiomyopathy, myocardial infarction, ischemia-reperfusion injury, abdominal aortic aneurysm, dissection, heart failure. Therefore, comprehensive understanding mechanisms that regulate ferroptosis diseases will enhance prevention treatment these diseases. This review discusses latest findings on molecular its regulation application modulators role traditional Chinese medicines to provide identify new options.
Language: Английский
Citations
9
Molecular Medicine, Journal Year: 2025, Volume and Issue: 31(1)
Published: Jan. 29, 2025
Language: Английский
Citations
1
Molecular and Cellular Biochemistry, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 17, 2025
Language: Английский
Citations
1