Renal function protection and the mechanism of ginsenosides: Current progress and future perspectives DOI Creative Commons

Meiling Fan,

Xintian Lan,

Qunling Wang

et al.

Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14

Published: Feb. 6, 2023

Nephropathy is a general term for kidney diseases, which refers to changes in the structure and function of caused by various factors, resulting pathological damage kidney, abnormal blood or urine components, other diseases. The main manifestations disease include hematuria, albuminuria, edema, hypertension, anemia, lower back pain, oliguria, symptoms. Early detection, diagnosis, active treatment are required prevent chronic renal failure. concept nephropathy encompasses wide range conditions, including acute injury, disease, nephritis, fibrosis, diabetic nephropathy. Some these kidney-related diseases interrelated may lead serious complications without effective control. In cases, it can also develop into dysfunction eventually end-stage disease. As result, seriously affects quality life patients places great economic burden on society families. Ginsenoside one components ginseng, with anti-inflammatory, anti-tumor, antioxidant, pharmacological activities. A variety monomers ginsenosides play protective roles multiple organs. According difference core structure, be divided protopanaxadiol-type (including Rb1, Rb3, Rg3, Rh2, Rd CK, etc.), protopanaxatriol (protopanaxatriol)- type Rg1, Rg2 Rh1, types Rg5, Rh4, Rh3, Rk1, Rk3, etc.). All showed significant protection, reduce models. This review summarizes reports protection mechanisms action injury

Language: Английский

FSP1: a key regulator of ferroptosis DOI Creative Commons
Wentao Li,

Longteng Liang,

Siyi Liu

et al.

Trends in Molecular Medicine, Journal Year: 2023, Volume and Issue: 29(9), P. 753 - 764

Published: June 24, 2023

Ferroptosis suppressor protein 1 (FSP1) is one of the main regulatory molecules ferroptosis. FSP1 functions through FSP1-coenzyme Q10 (CoQ10)-NAD(P)H axis and vitamin K redox cycle. regulated by upstream factors, including transcription factors noncoding RNA (ncRNA), subject to epigenetic modifications, which affect progress FSP1-related diseases. closely associated with poor prognosis malignant tumors plays an important role in disease treatment. This review aims provide a comprehensive understanding ferroptosis regulation summarizing pathways, possible mechanisms involving FSP1, relationship between

Language: Английский

Citations

110
GPX4, ferroptosis, and diseases DOI Open Access

Wangzheqi Zhang,

Yang Liu,

Liao Yan

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 174, P. 116512 - 116512

Published: April 3, 2024

GPX4 (Glutathione peroxidase 4) serves as a crucial intracellular regulatory factor, participating in various physiological processes and playing significant role maintaining the redox homeostasis within body. Ferroptosis, form of iron-dependent non-apoptotic cell death, has gained considerable attention recent years due to its involvement multiple pathological processes. is closely associated with ferroptosis functions primary inhibitor this process. Together, contribute pathophysiology several diseases, including sepsis, nervous system ischemia reperfusion injury, cardiovascular cancer. This review comprehensively explores roles impacts development progression these aim providing insights for identifying potential therapeutic strategies future.

Language: Английский

Citations

62
Pharmacological inhibition of ferroptosis as a therapeutic target for sepsis-associated organ damage DOI
Liang Huo, Chunfeng Liu,

Yujun Yuan

et al.

European Journal of Medicinal Chemistry, Journal Year: 2023, Volume and Issue: 257, P. 115438 - 115438

Published: May 13, 2023

Language: Английский

Citations

54
Ferroptosis inhibitors: past, present and future DOI Creative Commons
Lei Zhang, Yi Luo, Yang Xiang

et al.

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

Published: May 23, 2024

Ferroptosis is a non-apoptotic mode of programmed cell death characterized by iron dependence and lipid peroxidation. Since the ferroptosis was proposed, researchers have revealed mechanisms its formation continue to explore effective inhibitors in disease. Recent studies shown correlation between pathological neurodegenerative diseases, as well diseases involving tissue or organ damage. Acting on ferroptosis-related targets may provide new strategies for treatment ferroptosis-mediated diseases. This article specifically describes metabolic pathways summarizes reported action natural synthetic small molecule their efficacy The paper also treatments such gene therapy, nanotechnology, summarises challenges encountered clinical translation inhibitors. Finally, relationship other modes discussed, hopefully paving way future drug design discovery.

Language: Английский

Citations

20
Emerging significance and therapeutic targets of ferroptosis: a potential avenue for human kidney diseases DOI Creative Commons
Jinghan Li,

Sujuan Zheng,

Yumei Fan

et al.

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

Citations

28
Ferroptosis in acute kidney injury following crush syndrome: A novel target for treatment DOI Creative Commons

Ou Qiao,

Xinyue Wang, Yuru Wang

et al.

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

Citations

25
Ginsenoside Rg1 Suppresses Ferroptosis of Renal Tubular Epithelial Cells in Sepsis-induced Acute Kidney Injury via the FSP1-CoQ10- NAD(P)H Pathway DOI
Jun Guo, Long Chen, Min Ma

et al.

Current Medicinal Chemistry, Journal Year: 2023, Volume and Issue: 31(15), P. 2119 - 2132

Published: June 8, 2023

Introduction: Sepsis-induced acute kidney injury is related to an increased mortality rate by modulating ferroptosis through ginsenoside Rg1. In this study, we explored the specific mechanism of it. Methods: Human renal tubular epithelial cells (HK-2) were transfected with oe-ferroptosis suppressor protein 1 and treated lipopolysaccharide for induction, they then Rg1 inhibitor. Ferroptosis 1, CoQ10, CoQ10H2, intracellular NADH levels in HK-2 assessed Western blot, ELISA kit, NAD/NADH kit. NAD+/NADH ratio was also calculated, 4-Hydroxynonal fluorescence intensity immunofluorescence. cell viability death CCK-8 propidium iodide staining. Ferroptosis, lipid peroxidation, reactive oxygen species accumulation kits, flow cytometry, C11 BODIPY 581/591 molecular probe. Sepsis rat models established cecal ligation perforation investigate whether regulated 1-CoQ10-NAD(P)H pathway vivo. Results: LPS treatment diminished contents cells, while facilitating relative 4- Hydroxynonal intensity. FSP1 overexpression inhibited lipopolysaccharideinduced peroxidation via 1-CoQ10- NAD(P)H pathway. The suppressed lipopolysaccharide-induced cells. Ginsenoside alleviated regulating Moreover, Conclusion: sepsis-induced blocking

Language: Английский

Citations

24
SAP130 released by ferroptosis tubular epithelial cells promotes macrophage polarization via Mincle signaling in sepsis acute kidney injury DOI Creative Commons
Jing Zhang, Jun Jiang, Bingqing Wang

et al.

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

Citations

16
Ginsenoside Rg1 alleviates chronic inflammation-induced neuronal ferroptosis and cognitive impairments via regulation of AIM2 - Nrf2 signaling pathway DOI
Liangliang Kong, Yan Liu, Jingwei Li

et al.

Journal of Ethnopharmacology, Journal Year: 2024, Volume and Issue: 330, P. 118205 - 118205

Published: April 17, 2024

Language: Английский

Citations

16
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