Rusting from the inside: kidney-specific ferroportin deficiency and associated iron overload dictate susceptibility to acute kidney injury and fibrosis DOI
Yogesh Scindia

AJP Renal Physiology, Journal Year: 2024, Volume and Issue: 326(3), P. F497 - F498

Published: Jan. 11, 2024

Language: Английский

Oxidative cell death in cancer: mechanisms and therapeutic opportunities DOI Creative Commons
Xiaoqin An, Wenfeng Yu, Jinbao Liu

et al.

Cell Death and Disease, Journal Year: 2024, Volume and Issue: 15(8)

Published: Aug. 1, 2024

Abstract Reactive oxygen species (ROS) are highly reactive oxygen-containing molecules generated as natural byproducts during cellular processes, including metabolism. Under normal conditions, ROS play crucial roles in diverse functions, cell signaling and immune responses. However, a disturbance the balance between production antioxidant defenses can lead to an excessive buildup, causing oxidative stress. This stress damages essential components, lipids, proteins, DNA, potentially culminating death. form of death take various forms, such ferroptosis, apoptosis, necroptosis, pyroptosis, paraptosis, parthanatos, oxeiptosis, each displaying distinct genetic, biochemical, characteristics. The investigation holds promise for development pharmacological agents that used prevent tumorigenesis or treat established cancer. Specifically, targeting key SLC7A11, GCLC, GPX4, TXN, TXNRD, represents emerging approach inducing cancer cells. review provides comprehensive summary recent progress, opportunities, challenges therapy.

Language: Английский

Citations

75

Role of ferroptosis in chronic kidney disease DOI Creative Commons
Shiyang Li, Qiuxia Han, Chang Liu

et al.

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: Feb. 12, 2024

Abstract Chronic kidney disease (CKD) has historically been a significant global health concern, profoundly impacting both life and well-being. In the process of CKD, with gradual loss renal function, incidence various life-threatening complications, such as cardiovascular diseases, cerebrovascular accident, infection stroke, is also increasing rapidly. Unfortunately, existing treatments exhibit limited ability to halt progression injury in emphasizing urgent need delve into precise molecular mechanisms governing occurrence development CKD while identifying novel therapeutic targets. Renal fibrosis, typical pathological feature plays pivotal role disrupting normal structures function. Ferroptosis recently discovered iron-dependent form cell death characterized by lipid peroxide accumulation. emerged potential key player diseases initiation organ fibrosis. Substantial evidence suggests that ferroptosis may significantly contribute intricate interplay between its progression. This review comprehensively outlines relationship terms iron metabolism peroxidation, discusses current landscape pharmacological research on ferroptosis, shedding light promising avenues for intervention. It further illustrates recent breakthroughs ferroptosis-related regulatory implicated thereby providing new insights treatment.

Language: Английский

Citations

15

The role of epithelial cells in fibrosis: Mechanisms and treatment DOI Creative Commons

Liuyi Luo,

Wei Zhang,

Siyao You

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: 202, P. 107144 - 107144

Published: March 13, 2024

Fibrosis is a pathological process that affects multiple organs and considered one of the major causes morbidity mortality in diseases, resulting an enormous disease burden. Current studies have focused on fibroblasts myofibroblasts, which directly lead to imbalance generation degradation extracellular matrix (ECM). In recent years, increasing number role epithelial cells fibrosis. some cases, are first exposed external physicochemical stimuli may drive collagen accumulation mesenchyme. other source stimulation mainly immune cytokines, similarly altered process. this review, we will focus dynamic alterations involved after injury during fibrogenesis, discuss association among them, summarize therapies targeting changed cells. Especially, mesenchymal transition (EMT) key central step, closely linked biological behaviors. Meanwhile, think disruption barrier, cell death basal stem populations stemness fibrosis not appreciated. We believe targeted can prevent progress fibrosis, but reverse it. The provide wonderful preventive delaying action.

Language: Английский

Citations

10

Inhibition of tubular epithelial cells ferroptosis alleviates renal interstitial fibrosis by reducing lipid hydroperoxides and TGF-β/Smad signaling DOI Creative Commons
Yuting Chen, Yue Dai, Yi Huang

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: Feb. 11, 2025

Ferroptosis is a non-apoptotic form of regulated cell death that involves an imbalance in the homeostasis two elements: iron and lipid hydroperoxides. The accumulation hydroperoxide serves as key trigger for initiating ferroptosis. Recent studies have identified ferroptosis critical pathophysiology contributing to kidney disease progression. However, specific mechanisms underlying role chronic (CKD) not been elucidated. Tubular epithelial cells (TECs) was evaluated unilateral ureteral obstruction (UUO) models TGF-β-treated HK-2 explore relationship between fibrosis. inhibitors (ferrostatin-1) TECs-targeted glutathione peroxidase 4 (GPX4) overexpression vivo vitro were used investigate effect mechanism TECs on fibrosis Our findings indicate persistently activated during various states UUO model. As results, core facilitator renal interstitial UUO. reduction significantly ameliorated maintained structure proximal tubules. Persistent activation effectively aggravated progression through TGF-β/Smad pathway. Inhibiting rescues profibrotic cytokines, thereby alleviating closely related pathway, targeting increasing GPX4 expression could be effective strategy treating CKD. occurrence CKD due regulation, which drives peroxidation hydroperoxide. One primary drivers ferroptosis, peroxidation, further stimulates signaling exacerbates Abbreviations: TFRC, transferrin receptor protein 1; DMT1, divalent metal transporter FPN, ferroportin; ACSL4, acyl-CoA synthetase long-chain family 4; LPCAT3, lysophosphatidylcholine acyltransferase 3; GPX4, CTGF, connective tissue growth factor; PDGFB, platelet-derived factor subunit b; FGF2, fibroblast 2; TECs, tubular cells; CKD, disease. (The figure drawn with BioRender.)

Language: Английский

Citations

1

Kidney tea [Orthosiphon aristatus (Blume) Miq.] improves diabetic nephropathy via regulating gut microbiota and ferroptosis DOI Creative Commons
Zheng Zhou, Hongjuan Niu, Meng Bian

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: June 19, 2024

Introduction Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Due to its complex pathogenesis, new therapeutic agents are urgently needed. Orthosiphon aristatus (Blume) Miq., commonly known as kidney tea, widely used in DN treatment China. However, mechanisms have not been fully elucidated. Methods We db/db mice model and evaluated efficacy tea by measuring fasting blood glucose (FBG), serum inflammatory cytokines, injury indicators histopathological changes. Furthermore, 16S rDNA gene sequencing, untargeted metabolomics, electron microscope, ELISA, qRT-PCR, Western blotting were performed explore which exerted effects. Results Twelve polyphenols identified from extract ameliorated FBG, inflammation mice. Moreover, reshaped gut microbiota, reduced abundance Muribaculaceae , Lachnoclostridium Prevotellaceae_UCG-001 Corynebacterium Akkermansia enriched Alloprevotella Blautia Lachnospiraceae_NK4A136_group . Kidney altered levels metabolites pathways such ferroptosis, arginine biosynthesis mTOR signaling pathway. Importantly, improved mitochondrial damage, increased SOD activity, decreased MDA 4-HNE tissues Meanwhile, this functional upregulated GPX4 FTH1 expression downregulated ACSL4 NCOA4 expression, indicating that it could inhibit ferroptosis kidneys. Conclusion Our findings imply can attenuate development modulating microbiota presents a novel scientific rationale for clinical application tea.

Language: Английский

Citations

7

XueBiJing injection improves the symptoms of sepsis-induced acute lung injury by mitigating oxidative stress and ferroptosis DOI

Fanmei Zou,

Jing Zou,

Qiuzheng Du

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 337, P. 118732 - 118732

Published: Aug. 23, 2024

Language: Английский

Citations

7

Increased NPM1 inhibit ferroptosis and aggravate renal fibrosis via Nrf2 pathway in chronic kidney disease DOI Creative Commons

Wenjing Fu,

Mingyu Zhang, Yilin Meng

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2024, Volume and Issue: 1871(1), P. 167551 - 167551

Published: Oct. 20, 2024

Language: Английский

Citations

5

Proteomic and lipidomic analysis of the mechanism underlying astragaloside IV in mitigating ferroptosis through hypoxia-inducible factor 1α/heme oxygenase 1 pathway in renal tubular epithelial cells in diabetic kidney disease DOI
Jun Liu, Jing Ren,

Linlan Zhou

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 334, P. 118517 - 118517

Published: July 6, 2024

Language: Английский

Citations

4

Nanomedicines Targeting Ferroptosis to Treat Stress-Related Diseases DOI Creative Commons
Hao Kang,

Fansu Meng,

Fengjie Liu

et al.

International Journal of Nanomedicine, Journal Year: 2024, Volume and Issue: Volume 19, P. 8189 - 8210

Published: Aug. 1, 2024

Ferroptosis, a unique form of regulated cell death driven by iron-dependent lethal lipid peroxidation, is implicated in various stress-related diseases like neurodegeneration, vasculopathy, and metabolic disturbance. Stress-related encompass widespread medical disorders that are influenced or exacerbated stress. These stressors can manifest organ tissue systems have significant implications for human overall health. Understanding ferroptosis these offers insights therapeutic strategies targeting relevant pathways. This review explores mechanisms, its role pathophysiology, connection to diseases, the potential ferroptosis-targeted nanomedicines treating conditions. monograph also delves into engineering tackling including cancer, cardia-cerebrovascular, neurodegenerative, inflammatory diseases. Anyhow, nanotherapy holds promise both promoting suppressing managing

Language: Английский

Citations

4

Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions DOI Creative Commons
Mengmeng Wang, De-Gang Mo, Ning Zhang

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(15), P. e35219 - e35219

Published: July 28, 2024

Diabetic cardiomyopathy (DCM) is a common complication of diabetes, and its pathogenesis remains elusive. Ferroptosis, process dependent on iron-mediated cell death, plays crucial role in DCM via disrupted iron metabolism, lipid peroxidation, weakened antioxidant defenses. Hyperglycemia, oxidative stress, inflammation may exacerbate ferroptosis diabetes. This review emphasizes the interaction between cardiac fibroblasts cardiomyocytes DCM, influencing occurrence. By exploring modulation for potential therapeutic targets, this article offers fresh perspective treatment. The study systematically covers interplay, mechanisms, targeted drugs linked to development.

Language: Английский

Citations

4