Ferroptosis, a Rising Force against Renal Fibrosis

Oxidative Medicine and Cellular Longevity, Journal Year: 2022, Volume and Issue: 2022, P. 1 - 12

Published: Oct. 12, 2022

Ferroptosis is a type of programmed cell death characterized by iron overload, oxidative stress, imbalance in lipid repair, and mitochondria-specific pathological manifestations. Growing number molecular mechanisms signaling pathways have been found to be involved ferroptosis progression, including metabolism, amino acid energy metabolism. It worth noting that the progression fibrotic diseases such as liver cirrhosis, cardiomyopathy, idiopathic pulmonary fibrosis, inhibition has acquired beneficial outcomes rodent models, while studies on renal fibrosis remains limited. Recent revealed targeting can effectively mitigate chronic kidney injury fibrosis. Moreover, myofibroblasts suffer from during fiber extracellular matrix deposition cascade reaction pharmacological modulation shows great therapeutic effect Here, we summarize latest high-quality review its potential

Language: Английский

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miR-26a-5p Attenuates Oxidative Stress and Inflammation in Diabetic Retinopathy through the USP14/NF-κB Signaling Pathway

Journal of Ophthalmology, Journal Year: 2024, Volume and Issue: 2024, P. 1 - 15

Published: Jan. 19, 2024

Purpose. Diabetic retinopathy (DR) is an ocular disease caused by diabetes and may lead to vision impairment even blindness. Oxidative stress inflammation are two key pathogenic factors of DR. Recently, regulatory roles different microRNAs (miRNAs) in DR have been widely verified. miR-26a-5p has confirmed be a potential biomarker Nevertheless, the specific functions still unclear. Methods. Primary cultured mouse retinal Müller cells exposure high glucose (HG) were used establish vitro model. identified via morphology observation under phase contrast microscope fluorescence staining for glutamine synthetase. The vivo animal models constructed using streptozotocin-induced diabetic C57BL/6 mice. Western blotting was performed quantify cytochrome c protein level cytoplasm mitochondria measure levels glial fibrillary acidic (GFAP), ubiquitin-specific peptidase 14 (USP14), as well associated with NF-κB signaling (p-IκBα, IκBα, p- $\mathrm{p}65$ , id="M2">p65 nuclear translocation cells. Furthermore, interaction between USP14 verified luciferase reporter assays. Results. HG stimulation contributed cell dysfunction inducing inflammation, injury, mitochondrial damage downregulated condition, overexpression relieved HG-induced dysfunction. Moreover, targeted inversely regulated expression. Additionally, HG-evoked activation suppressed knockdown upregulation. Rescue assays showed that protective impact upregulation against reversed overexpression. retinas mice experiments. Injection agomir improved injury weakened cytokines Conclusion. inhibits progression targeting inactivating pathway.

Language: Английский

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Mutant NPM1-regulated lncRNA HOTAIRM1 promotes leukemia cell autophagy and proliferation by targeting EGR1 and ULK3

Journal of Experimental & Clinical Cancer Research, Journal Year: 2021, Volume and Issue: 40(1)

Published: Oct. 6, 2021

Acute myeloid leukemia (AML) with mutated nucleophosmin (NPM1), which displays a distinct long noncoding RNA (lncRNA) expression profile, has been defined as unique subgroup in the new classification of neoplasms. However, biological roles key lncRNAs development NPM1-mutated AML are currently unclear. Here, we aimed to investigate functional and mechanistic lncRNA HOTAIRM1 AML.The was analyzed public database further determined by qRT-PCR samples cell lines. The cause upregulated investigated luciferase reporter, chromatin immunoprecipitation ubiquitination assays. role autophagy proliferation evaluated using western blot analysis, immunofluorescence staining, Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2'-deoxyuridine (EdU) incorporation flow cytometric analyses animal studies. action mechanism explored through fluorescence situ hybridization, pulldown assays.HOTAIRM1 highly expressed AML. High induced part mutant NPM1 via KLF5-dependent transcriptional regulation. Importantly, promoted both vitro vivo. Mechanistic investigations demonstrated that nuclear EGR1 degradation serving scaffold facilitate MDM2-EGR1 complex formation, while cytoplasmic acted sponge for miR-152-3p increase ULK3 expression.Taken together, our findings identify two oncogenic regulatory axes centered on HOTAIRM1: one involving MDM2 nucleus other miR-152-3p/ULK3 axis cytoplasm. Our study indicates may be promising therapeutic target this subtype.

Language: Английский

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Roles and functions of antisense lncRNA in vascular aging

Ageing Research Reviews, Journal Year: 2021, Volume and Issue: 72, P. 101480 - 101480

Published: Oct. 1, 2021

Language: Английский

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Lnc Tmem235 promotes repair of early steroid-induced osteonecrosis of the femoral head by inhibiting hypoxia-induced apoptosis of BMSCs

Experimental & Molecular Medicine, Journal Year: 2022, Volume and Issue: 54(11), P. 1991 - 2006

Published: Nov. 16, 2022

Abstract Bone marrow mesenchymal stem cells (BMSCs) have been used in the treatment of early steroid-induced osteonecrosis femoral head (SONFH). However, hypoxic microenvironment osteonecrotic area leads to hypoxia-induced apoptosis transplanted BMSCs, which limits their efficacy. Therefore, approaches that inhibit BMSCs are promising for augmenting efficacy BMSC transplantation. Our present study found under hypoxia, expression long noncoding RNA (Lnc) transmembrane protein 235 (Tmem235) was downregulated, Bcl-2-associated X upregulated, B-cell lymphoma-2 and apoptotic rate over 70%. overexpression Lnc Tmem235 reversed promoted survival. These results demonstrated effectively inhibited BMSCs. Mechanistically, we exhibited competitive binding miR-34a-3p compared with BIRC5 mRNA, is an inhibitor apoptosis; this relieved silencing effect on mRNA ultimately by promoting BIRC5. Furthermore, cocultured overexpressing xenogeneic antigen-extracted cancellous bone construct tissue-engineered repair a model SONFH vivo. The showed reduced improved Taken together, our findings show regulating miR-34a-3p/BIRC5 axis, thus improving transplantation treating SONFH.

Language: Английский

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Roles of ubiquitin-specific proteases in inflammatory diseases

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

Published: Jan. 22, 2024

Ubiquitin-specific proteases (USPs), as one of the deubiquitinating enzymes (DUBs) families, regulate fate proteins and signaling pathway transduction by removing ubiquitin chains from target proteins. USPs are essential for modulation a variety physiological processes, such DNA repair, cell metabolism differentiation, epigenetic modulations well protein stability. Recently, extensive research has demonstrated that exert significant impact on innate adaptive immune reactions, metabolic syndromes, inflammatory disorders, infection via post-translational modification processes. This review summarizes important roles in onset progression diseases, including periodontitis, pneumonia, atherosclerosis, bowel disease, sepsis, hepatitis, diabetes, obesity. Moreover, we highlight comprehensive overview pathogenesis these diseases modifications responses pave way future prospect targeted therapies diseases.

Language: Английский

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Mechanisms and implications of podocyte autophagy in chronic kidney disease

AJP Renal Physiology, Journal Year: 2024, Volume and Issue: 326(6), P. F877 - F893

Published: April 11, 2024

Autophagy is a protective mechanism through which cells degrade and recycle proteins organelles to maintain cellular homeostasis integrity. An accumulating body of evidence underscores the significant impact dysregulated autophagy on podocyte injury in chronic kidney disease (CKD). In this review, we provide comprehensive overview diverse types their regulation homeostasis, with specific emphasis podocytes. Furthermore, discuss recent findings that focus functional role different during disease. The intricate interplay between health requires further research, critical for understanding pathogenesis CKD developing targeted therapeutic interventions.

Language: Английский

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Podocyte programmed cell death in diabetic kidney disease: Molecular mechanisms and therapeutic prospects

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 177, P. 117140 - 117140

Published: July 16, 2024

Language: Английский

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Human β-defensin-1 affects the mammalian target of rapamycin pathway and autophagy in colon cancer cells through long non-coding RNA TCONS_00014506

World Journal of Gastrointestinal Oncology, Journal Year: 2024, Volume and Issue: 16(4), P. 1465 - 1478

Published: April 9, 2024

Colorectal cancer has a low 5-year survival rate and high mortality. Human β-defensin-1 (hBD-1) may play an integral function in the innate immune system, contributing to recognition destruction of cells. Long non-coding RNAs (lncRNAs) are involved process cell differentiation growth.

Language: Английский

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Diabetes and Its Cardiovascular Complications: Comprehensive Network and Systematic Analyses

Frontiers in Cardiovascular Medicine, Journal Year: 2022, Volume and Issue: 9

Published: Feb. 17, 2022

Diabetes mellitus is a worldwide health problem that usually comes with severe complications. There no cure for diabetes yet and the threat of these complications what keeps researchers investigating mechanisms treatments mellitus. Due to advancements in genomics, epigenomics, proteomics, single-cell multiomics research, considerable progress has been made toward understanding In addition, investigation association between other physiological systems revealed potentially novel pathways targets involved initiation diabetes. This review focuses on current studying by using genomic, epigenomic, proteomic, multiomic analysis methods. It will also focus recent findings pertaining relationship biological processes, new contribution several pathological conditions.

Language: Английский

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