Oxidative Stress, Reductive Stress and Antioxidants in Vascular Pathogenesis and Aging

Antioxidants, Journal Year: 2023, Volume and Issue: 12(5), P. 1126 - 1126

Published: May 19, 2023

This review is focused on the mechanisms that regulate health, disease and aging redox status, signal pathways counteract oxidative reductive stress, role of food components additives with antioxidant properties (curcumin, polyphenols, vitamins, carotenoids, flavonoids, etc.), hormones irisin melatonin in homeostasis animal human cells. The correlations between deviation from optimal conditions inflammation, allergic, autoimmune responses are discussed. Special attention given to vascular system, kidney, liver brain stress processes. hydrogen peroxide as an intracellular paracrine molecule also reviewed. cyanotoxins β-N-methylamino-l-alanine (BMAA), cylindrospermopsin, microcystins nodularins introduced potentially dangerous environment pro-oxidants.

Language: Английский

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Salidroside ameliorates acetaminophen-induced acute liver injury through the inhibition of endoplasmic reticulum stress-mediated ferroptosis by activating the AMPK/SIRT1 pathway

Ecotoxicology and Environmental Safety, Journal Year: 2023, Volume and Issue: 262, P. 115331 - 115331

Published: Aug. 7, 2023

Acetaminophen (APAP) overdose has long been considered a major cause of drug-induced liver injury. Ferroptosis is type programmed cell death mediated by iron-dependent lipid peroxidation. Endoplasmic reticulum (ER) stress systemic response triggered the accumulation unfolded or misfolded proteins in ER. and ER have proven to contribute progression APAP-induced acute injury (ALI). It was reported that salidroside protects against ALI, but potential mechanism remain unknown. In this study, male C57BL/6 J mice were intraperitoneally (i.p.) injected APAP (500 mg/kg) induce an ALI model. Salidroside i.p. at dose 100 mg/kg 2 h prior administration. Mice sacrificed 12 after injection serum obtained for histological biochemistry analysis. AML12 cells used vitro assays. The results indicated mitigated glutathione degradation via inhibiting cation transport regulator homolog 1 (CHAC1) attenuate ferroptosis, simultaneously suppressing PERK-eIF2α-ATF4 axis-mediated stress, thus alleviating ALI. However, PERK activator CCT020312 overexpression ATF4 inhibited protective function on CHAC1-mediated ferroptosis. Besides this, activation AMPK/SIRT1 signaling pathway demonstrated effect Interestingly, selective inhibition SIRT1 ameliorated effects Overall, plays significant part mitigation activating inhibit stress-mediated ferroptosis ATF4-CHAC1 axis.

Language: Английский

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Emerging significance and therapeutic targets of ferroptosis: a potential avenue for human kidney diseases

Cell Death and Disease, Journal Year: 2023, Volume and Issue: 14(9)

Published: Sept. 22, 2023

Abstract Kidney diseases remain one of the leading causes human death and have placed a heavy burden on medical system. Regulated cell contributes to pathology plethora renal diseases. Recently, with in-depth studies into kidney death, new iron-dependent modality, known as ferroptosis, has been identified attracted considerable attention among researchers in pathogenesis therapeutics treat them. The majority suggest that ferroptosis plays an important role pathologies multiple diseases, such acute injury (AKI), chronic disease, carcinoma. In this review, we summarize recently regulatory molecular mechanisms discuss pathways action various describe protective effect inhibitors against especially AKI. By summarizing prominent roles different progress made studying provide directions strategies for future research summary, ferroptotic factors are potential targets therapeutic intervention alleviate targeting them may lead treatments patients

Language: Английский

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Irisin as an agent for protecting against osteoporosis: A review of the current mechanisms and pathways

Journal of Advanced Research, Journal Year: 2023, Volume and Issue: 62, P. 175 - 186

Published: Sept. 3, 2023

Osteoporosis is recognized as a skeletal disorder characterized by diminished bone tissue quality and density. Regular physical exercise widely acknowledged to preserve enhance health, but the detailed molecular mechanisms involved remain unclear. Irisin, factor derived from muscle during exercise, influences muscle. Since its discovery in 2012, irisin has been found promote growth reduce resorption, establishing tangible link between exertion health. Consequently, mechanism which prevents osteoporosis have attracted significant scientific interest.

Language: Английский

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Ferroptosis and cuproptposis in kidney Diseases: dysfunction of cell metabolism

APOPTOSIS, Journal Year: 2023, Volume and Issue: 29(3-4), P. 289 - 302

Published: Dec. 14, 2023

Metal ions play an important role in living organisms and are involved essential physiological activities. However, the overload state of can cause excess free radicals, cell damage, even death. Ferroptosis cuproptosis specific forms death that distinct from apoptosis, necroptosis, other regulated These unique modalities death, dependent on iron copper, by multiple cellular metabolic pathways, including steady-state metal redox treatment mitochondrial activity lipid, amino acid glucose metabolism, various signaling pathways associated with disease. Although mechanisms ferroptosis not yet fully understood, there is no doubt ion plays a crucial act these metal-dependent deaths. In this review, we discussed core roles cuproptosis, association between metabolism imbalance extract diseases caused current modalities.

Language: Английский

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Ferroptosis in acute kidney injury following crush syndrome: A novel target for treatment

Journal of Advanced Research, Journal Year: 2023, Volume and Issue: 54, P. 211 - 222

Published: Jan. 23, 2023

Crush syndrome (CS) is a kind of traumatic and ischemic injury that seriously threatens life after prolonged compression. It characterized by systemic inflammatory reaction, myoglobinuria, hyperkalemia acute kidney (AKI). Especially AKI, it the leading cause death from CS. There are various cell forms in among which ferroptosis typical form death. However, role has not been fully revealed CS-AKI. This review aimed to summarize evidence CS-AKI its related molecular mechanism, discuss therapeutic significance CS-AKI, open up new ideas for treatment One main pathological manifestations renal tubular epithelial dysfunction death, attributed massive deposition myoglobin. Large amounts myoglobin released damaged muscle deposited tubules, impeding normal tubules function directly damaging with oxidative stress elevated iron levels. Lipid peroxidation damage overload distinguishing features ferroptosis. Moreover, high levels pro-inflammatory cytokines damage-associated molecule pattern molecules (HMGB1, double-strand DNA, macrophage extracellular trap) tissue have shown promote how occurs whether can be target remains unclear. In our current work, we systematically reviewed occurrence underlying mechanism

Language: Английский

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Irisin drives macrophage anti-inflammatory differentiation via JAK2-STAT6-dependent activation of PPARγ and Nrf2 signaling

Free Radical Biology and Medicine, Journal Year: 2023, Volume and Issue: 201, P. 98 - 110

Published: March 20, 2023

Language: Английский

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SAP130 released by ferroptosis tubular epithelial cells promotes macrophage polarization via Mincle signaling in sepsis acute kidney injury

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 129, P. 111564 - 111564

Published: Feb. 5, 2024

The pathological mechanism of sepsis-associated acute kidney injury (SA-AKI) is complex and involves tubular epithelial cell (TEC) death immune activation. However, the interaction between macrophage-mediated inflammation remains unclear. In this study, we uncovered that TEC ferroptosis was activated in SA-AKI. Increased levels ferroptotic markers, including ferroptosis-related proteins, lipid peroxidation, malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), reactive oxygen species (ROS), mitochondrial damage, were observed tissue cecum ligation puncture (CLP) Lipopolysaccharide (LPS)-induced SA-AKI mouse models, which subsequently suppressed by Ferrostatin-1 (Fer-1). vitro experiments showed Fer-1 inhibits LPS-induced Fe2+ accumulation, cytosolic ROS production. Moreover, it found induced promoted macrophage-inducible C-type lectin (Mincle) its downstream expression M1 polarization, mediated release spliceosome-associated protein 130 (SAP130), an endogenous ligand Mincle, from TEC. It confirmed supernatant LPS-stimulated TECs Mincle polarization macrophages. Further revealed macrophages aggravated ferroptosis, offset neutralizing SAP130 or inhibiting expression. addition, circulatory blunted expression, as well macrophage infiltration mice. conclusion, triggering Mincle/syk/NF-κB signaling, macrophages, turn, ferroptosis.

Language: Английский

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Andrographolide attenuates sepsis-induced acute kidney injury by inhibiting ferroptosis through the Nrf2/FSP1 pathway

Free Radical Research, Journal Year: 2024, Volume and Issue: 58(3), P. 156 - 169

Published: March 3, 2024

Sepsis is a systemic inflammatory response syndrome caused by infection, which causes renal dysfunction known as sepsis-associated acute kidney injury (S-AKI). Ferroptosis form of lipid peroxidation dependent on iron and reactive oxygen species that differs from other forms programmed cell death at the morphological biochemical levels. Andrographolide (AG), natural diterpenoid lactone compound extracted Andrographis paniculata, has been shown to have therapeutic effects in disease. In this study, we investigated novel mechanism AG attenuates septic inhibiting ferroptosis tubular epithelial cells (HK-2) through Nrf2/FSP1 pathway. Cecum ligation puncture (CLP)-induced rats LPS-induced HK-2 were used for vivo vitro experiments. Firstly, cells, effectively decreased levels indicators including blood creatinine, urea nitrogen, markers such neutrophil gelatinase-associated transport protein (NGAL) molecule-1 (KIM-1). addition, prevented ferroptotosis, avoiding accumulation peroxidation, an increase SLC7A11 GPX4 AG-treated cells. Furthermore, attenuated mitochondrial damage, swelling, outer membrane rupture, reduction cristae LPS-treated Ferrostatin-1 (Fer-1), inhibitor, significantly inhibited Importantly, our results confirm important pathway resistance. Nrf2 siRNA hindered effect attenuating ferroptosis. These findings demonstrate Nrf2/FSP1-mediated associated with AG, alleviates injury, indicates avenue interventions treatment sepsis.

Language: Английский

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Crosstalk between Endoplasmic Reticulum Stress and Ferroptosis in Liver Diseases

Frontiers in Bioscience-Landmark, Journal Year: 2024, Volume and Issue: 29(6), P. 221 - 221

Published: June 20, 2024

The endoplasmic reticulum (ER) played an important role in the folding, assembly and post-translational modification of proteins. ER homeostasis could be disrupted by accumulation misfolded proteins, elevated reactive oxygen species (ROS) levels, abnormal Ca2+ signaling, which was referred to stress (ERS). Ferroptosis a unique programmed cell death model mediated iron-dependent phospholipid peroxidation multiple signaling pathways. changes mitochondrial structure, damage glutathione peroxidase 4 (GPX4) excess iron were main characteristics ferroptosis. ROS produced ferroptosis can interfere with activity protein-folding enzymes, leading large amounts unfolded thus causing ERS. On contrary, increase ERS level promote ion lipid peroxide, up-regulation related genes. At present, studies on relationship between one-sided lack in-depth interaction mechanism. This review aimed explore molecular mechanism cross-talk ERS, provide new strategies targets for treatment liver diseases.

Language: Английский

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