Molecular and metabolic responses to immune stress in the jejunum of broiler chickens: transcriptomic and metabolomic analysis DOI Creative Commons
Weidong Hu,

Lin Du,

Jianjian Shao

и другие.

Poultry Science, Год журнала: 2024, Номер 103(5), С. 103621 - 103621

Опубликована: Март 6, 2024

In the large poultry industry, where farmed chickens are fed at high density, prevalence of pathogens and repeated vaccinations induce immune stress, which can significantly decrease production performance increase mortality. This study was designed to shed light on molecular mechanisms metabolic pathways involved in stress through an in-depth analysis transcriptomic metabolomic changes jejunum samples from broilers. Two groups were established for experiment: a control group LPS group. received intraperitoneal injection solution dose 250 μg per kg 12, 14, 33, 35 days age, whereas sterile saline injection. The severity assessed using Disease Activity Index. A jejunal section collected measure intestinal villus structure (villus length crypt depth). RNA sequencing metabolomics data conducted reveal differentially expressed genes metabolites. results showed that DAI index increased height/crypt depth decreased total 96 672 accumulating metabolites detected by compared comprehensive 23 enriched appetite, nutrient absorption, energy substance metabolism disorders ferroptosis play important role Our findings provide deeper understanding responses broilers LPS-induced suggesting potential targets therapeutic strategies improve broiler chickens.

Язык: Английский

Molecular mechanisms of ferroptosis and relevance to inflammation DOI Open Access

Liyan Deng,

Shasha He,

Nuoqing Guo

и другие.

Inflammation Research, Год журнала: 2022, Номер 72(2), С. 281 - 299

Опубликована: Дек. 19, 2022

Язык: Английский

Процитировано

131

Empagliflozin attenuates the renal tubular ferroptosis in diabetic kidney disease through AMPK/NRF2 pathway DOI

QianYu Lu,

LiJiao Yang,

Jing‐Jie Xiao

и другие.

Free Radical Biology and Medicine, Год журнала: 2022, Номер 195, С. 89 - 102

Опубликована: Дек. 27, 2022

Язык: Английский

Процитировано

98

Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases DOI Creative Commons
Yumin Wang, Jing Hu, Shuang Wu

и другие.

Signal Transduction and Targeted Therapy, Год журнала: 2023, Номер 8(1)

Опубликована: Дек. 10, 2023

Abstract Ferroptosis, a unique modality of cell death with mechanistic and morphological differences from other modes, plays pivotal role in regulating tumorigenesis offers new opportunity for modulating anticancer drug resistance. Aberrant epigenetic modifications posttranslational (PTMs) promote resistance, cancer progression, metastasis. Accumulating studies indicate that can transcriptionally translationally determine vulnerability to ferroptosis functions as driver nervous system diseases (NSDs), cardiovascular (CVDs), liver diseases, lung kidney diseases. In this review, we first summarize the core molecular mechanisms ferroptosis. Then, roles processes, including histone PTMs, DNA methylation, noncoding RNA regulation such phosphorylation, ubiquitination, SUMOylation, acetylation, ADP-ribosylation, are concisely discussed. The PTMs genesis cancers, NSD, CVDs, well application PTM modulators therapy these then discussed detail. Elucidating mediated by will facilitate development promising combination therapeutic regimens containing or PTM-targeting agents inducers be used overcome chemotherapeutic resistance could prevent addition, highlight potential approaches chemoresistance halt

Язык: Английский

Процитировано

72

Ferroptosis in health and disease DOI Creative Commons
Carsten Berndt, Hamed Alborzinia,

Vera Skafar Amen

и другие.

Redox Biology, Год журнала: 2024, Номер 75, С. 103211 - 103211

Опубликована: Май 30, 2024

Ferroptosis is a pervasive non-apoptotic form of cell death highly relevant in various degenerative diseases and malignancies. The hallmark ferroptosis uncontrolled overwhelming peroxidation polyunsaturated fatty acids contained membrane phospholipids, which eventually leads to rupture the plasma membrane. unique that it essentially spontaneous, uncatalyzed chemical process based on perturbed iron redox homeostasis contributing process, but nonetheless modulated by many metabolic nodes impinge cells' susceptibility ferroptosis. Among affecting sensitivity, several have emerged as promising candidates for pharmacological intervention, rendering ferroptosis-related proteins attractive targets treatment numerous currently incurable diseases. Herein, current members Germany-wide research consortium focusing research, well key external experts who made seminal contributions this rapidly growing exciting field gathered provide comprehensive, state-of-the-art review Specific topics include: basic mechanisms, vivo relevance, specialized methodologies, tools, potential contribution disease etiopathology progression. We hope article will not only established scientists newcomers with an overview multiple facets ferroptosis, also encourage additional efforts characterize further molecular pathways modulating ultimate goal develop novel pharmacotherapies tackle associated - or caused

Язык: Английский

Процитировано

62

Rhein attenuates cerebral ischemia-reperfusion injury via inhibition of ferroptosis through NRF2/SLC7A11/GPX4 pathway DOI
Hua Liu,

Tian-ai Zhang,

Wen-Yue Zhang

и другие.

Experimental Neurology, Год журнала: 2023, Номер 369, С. 114541 - 114541

Опубликована: Сен. 13, 2023

Язык: Английский

Процитировано

57

Mechanisms and regulations of ferroptosis DOI Creative Commons

Xu-Dong Zhang,

Zhongyuan Liu,

Mao-Sen Wang

и другие.

Frontiers in Immunology, Год журнала: 2023, Номер 14

Опубликована: Окт. 6, 2023

Regulation of cell mortality for disease treatment has been the focus research. Ferroptosis is an iron-dependent regulated death whose mechanism extensively studied since its discovery. A large number studies have shown that regulation ferroptosis brings new strategies various benign and malignant diseases. Iron excess lipid peroxidation are primary metabolic features. Therefore, genes involved in iron metabolism can regulate overload through direct or indirect pathways, thereby regulating ferroptosis. In addition, glutathione (GSH) body’s non-enzymatic antioxidants plays a pivotal role struggle against peroxidation. GSH functions as auxiliary substance peroxidase 4 (GPX4) to convert toxic peroxides their corresponding alcohols. Here, we reviewed researches on recent years, comprehensively analyzed regulatory process from metabolism, then described detail GPX4 main antioxidant vivo .

Язык: Английский

Процитировано

51

Research on ferroptosis as a therapeutic target for the treatment of neurodegenerative diseases DOI Creative Commons
Yi Wang,

Meng-nan Lv,

Weijiang Zhao

и другие.

Ageing Research Reviews, Год журнала: 2023, Номер 91, С. 102035 - 102035

Опубликована: Авг. 23, 2023

Ferroptosis is an iron- and lipid peroxidation (LPO)-mediated programmed cell death type. Recently, mounting evidence has indicated the involvement of ferroptosis in neurodegenerative diseases, especially Alzheimer's disease (AD), Parkinson's (PD), multiple sclerosis (MS), amyotrophic lateral (ALS), Huntington's (HD), so on. Treating presents opportunities as well challenges for diseases. This review provides a comprehensive overview underlying mechanisms that contribute to occurrence ferroptosis, their implications pathogenesis advancement major disorders. Meanwhile, we summarize interaction between other types diseases contribution corresponding drug development. In addition, specifically recent advances developing therapeutic means targeting these which may guide future approaches effective management devastating medical conditions.

Язык: Английский

Процитировано

47

Ferroptosis: a new hunter of hepatocellular carcinoma DOI Creative Commons

Yulang Jiang,

Yongxin Yu,

Ziyang Pan

и другие.

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

Опубликована: Март 13, 2024

Abstract Ferroptosis is an iron ion-dependent, regulatory cell death modality driven by intracellular lipid peroxidation that plays a key role in the development of HCC. Studies have shown various clinical agents (e.g., sorafenib) ferroptosis inducer-like effects and can exert therapeutic modulating different factors pathway. This implies targeting tumor may be very promising strategy for therapy. In this paper, we summarize prerequisites defense systems occurrence targets drug-mediated action HCC, differences connections between other programmed deaths. We aim to theoretical basis, classical inducers research progress HCC cells, clued treatment regulating network. Further investigation specific mechanisms hepatocellular carcinoma interventions at stages will help us deepen our understanding carcinoma, with view providing new more precise preventive as well measures patients.

Язык: Английский

Процитировано

20

rmMANF prevents sepsis-associated lung injury via inhibiting endoplasmic reticulum stress-induced ferroptosis in mice DOI Creative Commons
Tao Zeng, Yan Zhou, Yang Yu

и другие.

International Immunopharmacology, Год журнала: 2022, Номер 114, С. 109608 - 109608

Опубликована: Дек. 20, 2022

Ferroptosis plays a critical role in LPS-induced acute lung injury and is modulated by endoplasmic reticulum stress (ERS). As typical ER stress-responsive protein, recently mesencephalic astrocyte-derived neurotrophic factor (MANF) has been demonstrated to attenuate (ALI) through repressing macrophage activation. However, whether MANF exerts preventive on ferroptosis excess remains unclear. Here, we first built protein-protein interaction (PPI) network obtain potential interacting proteins related STRING GeneMANIA. Then, male C57BL/6J mice were used build model of injury. Two days before LPS injection, the tail vein injected recombinant murine (rmMANF) at 750 μg/kg. Twenty-four hours after histopathological changes damage tissues detected scored HE staining TUNEL assay, respectively. Endogenous levels, oxidative markers (GSH, SOD, CAT, MDA), ERS (GRP78, PERK, ATF4), (iron, GPX4, 4-HNE) measured IHC, western blotting, commercial kits. Our results showed that induced significant increase MPO, MDA, 4-HNE, decrease GPX4 GSH, total iron accumulation LPS-exposed mice. Simultaneously, GRP78/PERK/ATF4 pathway was notably activated LPS, accompanied down-regulation MANF. Furthermore, rmMANF pretreatment markedly prevented tissue characteristics with increased level sepsis Finally, found activation significantly restrained pretreatment, except for endogenous level. Overall, can prevent sepsis-associated inhibiting stress-induced

Язык: Английский

Процитировано

43

Resveratrol inhibits ferroptosis and decelerates heart failure progression via Sirt1/p53 pathway activation DOI Creative Commons
Wei Zhang, Shaohuan Qian, Bi Tang

и другие.

Journal of Cellular and Molecular Medicine, Год журнала: 2023, Номер 27(20), С. 3075 - 3089

Опубликована: Июль 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.

Язык: Английский

Процитировано

36