European Journal of Pharmacology, Год журнала: 2023, Номер 957, С. 176031 - 176031
Опубликована: Сен. 1, 2023
Язык: Английский
Frontiers in Immunology, Год журнала: 2022, Номер 13
Опубликована: Июль 22, 2022
Quercetin, a naturally non-toxic flavonoid within the safe dose range with antioxidant, anti-apoptotic and anti-inflammatory properties, plays an important role in treatment of aging-related diseases. Sirtuin 1 (SIRT1), member NAD+-dependent deacetylase enzyme family, is extensively explored as potential therapeutic target for attenuating aging-induced disorders. SIRT1 possess beneficial effects against diseases such Alzheimer's disease (AD), Parkinson's (PD), Huntington's (HD), Depression, Osteoporosis, Myocardial ischemia (M/I) reperfusion (MI/R), Atherosclerosis (AS), Diabetes. Previous studies have reported that aging increases tissue susceptibility, whereas, regulates cellular senescence multiple processes, including SIRT1/Keap1/Nrf2/HO-1 SIRTI/PI3K/Akt/GSK-3β mediated oxidative stress, SIRT1/NF-κB SIRT1/NLRP3 regulated inflammatory response, SIRT1/PGC1α/eIF2α/ATF4/CHOP SIRT1/PKD1/CREB controlled phosphorylation, SIRT1-PINK1-Parkin mitochondrial damage, SIRT1/FoxO autophagy, SIRT1/FoxG1/CREB/BDNF/Trkβ-catenin neuroprotective effects. In this review, we summarized improvement attenuation effect quercetin on relationship between relevant signaling pathways by SIRT1. Moreover, functional regulation markers function, autophagy apoptosis through was discussed. Finally, prospects extracellular vesicles (EVs) loading delivery, SIRT1-mediated EVs signal carriers treating diseases, well discussed ferroptosis alleviation to protect via activating Generally, may serve promising inhibiting reducing responses, restoring dysfunction.
Язык: Английский
Процитировано
207
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Год журнала: 2023, Номер 1878(3), С. 188890 - 188890
Опубликована: Март 29, 2023
Язык: Английский
Процитировано
204
Signal Transduction and Targeted Therapy, Год журнала: 2024, Номер 9(1)
Опубликована: Янв. 8, 2024
Abstract Ischemia-reperfusion (I/R) injury paradoxically occurs during reperfusion following ischemia, exacerbating the initial tissue damage. The limited understanding of intricate mechanisms underlying I/R hinders development effective therapeutic interventions. Wnt signaling pathway exhibits extensive crosstalk with various other pathways, forming a network system pathways involved in injury. This review article elucidates signaling, as well complex interplay between and including Notch, phosphatidylinositol 3-kinase/protein kinase B, transforming growth factor-β, nuclear factor kappa, bone morphogenetic protein, N-methyl-D-aspartic acid receptor-Ca 2+ -Activin A, Hippo-Yes-associated toll-like receptor 4/toll-interleukine-1 domain-containing adapter-inducing interferon-β, hepatocyte factor/mesenchymal-epithelial transition factor. In particular, we delve into their respective contributions to key pathological processes, apoptosis, inflammatory response, oxidative stress, extracellular matrix remodeling, angiogenesis, cell hypertrophy, fibrosis, ferroptosis, neurogenesis, blood-brain barrier damage Our comprehensive analysis reveals that activation canonical promotes organ recovery, while non-canonical exacerbates Moreover, explore novel approaches based on these mechanistic findings, incorporating evidence from animal experiments, current standards, clinical trials. objective this is provide deeper insights roles its I/R-mediated processes dysfunction, facilitate innovative agents for
Язык: Английский
Процитировано
152
Cell Death and Disease, Год журнала: 2022, Номер 13(2)
Опубликована: Фев. 24, 2022
Acute kidney injury (AKI) is a major public health problem with high incidence and mortality. As form of programmed cell death (PCD), ferroptosis could be considered as process iron accumulation enhanced lipid peroxidation. Recently, the fundamental roles in AKI have attracted much attention. The network mechanism its to chronic disease (CKD) transition complicated multifactorial. Strategies targeting show great potential. Here, we review research progress on participation AKI. We hope that this work will provide clues for further studies
Язык: Английский
Процитировано
126
Redox Biology, Год журнала: 2022, Номер 54, С. 102382 - 102382
Опубликована: Июнь 23, 2022
The side effects of cisplatin, a widely used chemotherapeutic agent, include nephrotoxicity. Previous studies have reported that cisplatin induces ferroptosis and lipid peroxide accumulation. Ferroptosis, type regulated cell death, is characterized by iron-dependent peroxidation. Although previous examined the regulation in acute kidney injury (AKI), regulatory mechanism has not been elucidated. Here, ability activated farnesoid X receptor (FXR) to attenuate cisplatin-induced AKI through was examined. FXR deficiency exhibited more responses, such as increase peroxidation, iron content heme oxygenase 1 protein, decrease glutathione/glutathione disulfide ratio glutathione peroxidase 4 levels HK2 cells mice. Increased blood urea nitrogen, serum creatinine, ferroptotic responses mouse model were mitigated upon treatment with agonist GW4064 but exacerbated knockout RNA sequencing analysis revealed ferroptosis-associated genes novel targets FXR. upregulated expression metabolism-related downregulated death-related genes. Additionally, chromatin immunoprecipitation assays, using mice renal tissues, agonist-activated could bind its known target (Slc51a, Slc51b, Osgin1, Mafg) ferroptosis-related (Aifm2, Ggt6, Gsta4). Furthermore, FXR-dependent MAFG, transcriptional repressor, Hmox1, Nqo1, Tf tissues agonist-treated These findings indicate regulates transcription protects against AKI.
Язык: Английский
Процитировано
102
Redox Biology, Год журнала: 2023, Номер 63, С. 102760 - 102760
Опубликована: Май 23, 2023
Cancer cells and ischemic diseases exhibit unique metabolic responses adaptations to energy stress. Forkhead box O 3a (FoxO3a) is a transcription factor that plays an important role in cell metabolism, mitochondrial dysfunction oxidative stress response. Although the AMP-activated protein kinase (AMPK)/FoxO3a signaling pathway pivotal maintaining homeostasis under conditions of stress, AMPK/FoxO3a mitochondria-associated ferroptosis has not yet been fully elucidated. We show glucose starvation induced activation inhibited by erastin. Inhibition AMPK or loss FoxO3a cancer condition can sensitize these ferroptosis. Glucose deprivation mitochondria-related gene expression, reduced DNA(mtDNA) copy number, decreased expression proteins lowered levels respiratory complexes inducing FoxO3a. Loss promoted membrane potential hyperpolarization, oxygen consumption, lipid peroxide accumulation abolished protective effects on vitro. In addition, we identified FDA-approved antipsychotic agent, potent agonist trifluoperazine, which largely ferroptosis-associated cerebral ischemia-reperfusion (CIR) injuries rats through AMPK/FoxO3a/HIF-1α mitochondria-dependent mechanisms. found binds promoters SLC7A11 reduces CIR-mediated glutamate excitotoxicity inhibiting SLC7A11. Collectively, results suggest modulation regulates activity alters The regulation may play crucial controls balance confers resistance CIR injuries.
Язык: Английский
Процитировано
59
Heliyon, Год журнала: 2024, Номер 10(3), С. e24786 - e24786
Опубликована: Янв. 19, 2024
Ferroptosis is a newly discovered non-apoptotic and iron-dependent type of cell death. mainly takes place owing to the imbalance anti-oxidation oxidation in body. It regulated via number factors pathways both inside outside cell. closely linked with brain various neurological disorders (NDs). In human body, contains highest levels polyunsaturated fatty acids, which are known as lipid peroxide precursors. addition, there also connection glutathione depletion peroxidation NDs. There growing evidence regarding possible link between neuroinflammation multiple NDs, such Alzheimer's disease, amyotrophic lateral sclerosis, Parkinson's Huntington's stroke. Recent studies have demonstrated that disruptions reactive oxygen species (ROS), glutamate excitatory toxicity, iron homeostasis, other manifestations ferroptosis can be identified neuroinflammation-mediated has been reported damage-associated molecular pattern molecules including ROS generated during events cause glial activation activating neuroimmune pathways, subsequently leads generation inflammatory play role This review summarizes regulation ferroptosis, well inflammation potential range therapeutic agents used target treatment disorders.
Язык: Английский
Процитировано
20
Antioxidants, Год журнала: 2022, Номер 11(11), С. 2196 - 2196
Опубликована: Ноя. 6, 2022
Ischemia-reperfusion (I/R) injury is a major challenge in perioperative medicine that contributes to pathological damage various conditions, including ischemic stroke, myocardial infarction, acute lung injury, liver transplantation, kidney and hemorrhagic shock. I/R often irreversible, current treatments for are limited. Ferroptosis, type of regulated cell death characterized by the iron-dependent accumulation lipid hydroperoxides, has been implicated multiple diseases, injury. Emerging evidence suggests ferroptosis can serve as therapeutic target alleviate pharmacological strategies targeting have developed models. Here, we systematically summarize recent advances research on provide comprehensive analysis ferroptosis-regulated genes investigated context I/R, well applications regulators, insights into developing this devastating disease.
Язык: Английский
Процитировано
65
Annual Review of Nutrition, Год журнала: 2022, Номер 42(1), С. 275 - 309
Опубликована: Июнь 2, 2022
Ferroptosis is a type of regulated cell death characterized by an excessive lipid peroxidation cellular membranes caused the disruption antioxidant defense system and/or imbalanced metabolism. differentiates from other forms in that several metabolic pathways and nutritional aspects, including endogenous antioxidants (such as coenzyme Q10, vitamin E, di/tetrahydrobiopterin), iron handling, energy sensing, selenium utilization, amino acids, fatty directly regulate cells' sensitivity to ferroptosis. As hallmarks ferroptosis have been documented variety diseases, neurodegeneration, acute organ injury, therapy-resistant tumors, modulation using pharmacological tools or reprogramming holds great potential for treatment ferroptosis-associated diseases cancer therapy. Hence, this review focuses on regulation cues discusses interventions therapy targeting
Язык: Английский
Процитировано
62
Free Radical Biology and Medicine, Год журнала: 2022, Номер 189, С. 122 - 135
Опубликована: Июль 14, 2022
Язык: Английский
Процитировано
52