LncRNA SNHG1 knockdown inhibits hyperglycemia induced ferroptosis viamiR‐16‐5p/ACSL4 axis to alleviate diabetic nephropathy DOI Creative Commons
Xiangdong Fang,

Jianling Song,

Yanxia Chen

et al.

Journal of Diabetes Investigation, Journal Year: 2023, Volume and Issue: 14(9), P. 1056 - 1069

Published: June 14, 2023

Hyperglycemia accelerates the development of diabetic nephropathy (DN) by inducing renal tubular injury. Nevertheless, mechanism has not been elaborated fully. Here, pathogenesis DN was investigated to seek novel treatment strategies.A model established in vivo, levels blood glucose, urine albumin creatinine ratio (ACR), creatinine, urea nitrogen (BUN), malondialdehyde (MDA), glutathione (GSH), and iron were measured. The expression detected qRT-PCR Western blotting. H&E, Masson, PAS staining used assess kidney tissue mitochondria morphology observed transmission electron microscopy (TEM). molecular interaction analyzed using a dual luciferase reporter assay.SNHG1 ACSL4 increased tissues mice, but miR-16-5p decreased. Ferrostatin-1 or SNHG1 knockdown inhibited ferroptosis high glucose (HG)-treated HK-2 cells db/db mice. Subsequently, confirmed be target for SNHG1, directly targeted ACSL4. Overexpression greatly reversed protective roles HG-induced cells.SNHG1 via miR-16-5p/ACSL4 axis alleviate nephropathy, which provided some new insights nephropathy.

Language: Английский

Interactions Among lncRNA/circRNA, miRNA, and mRNA in Musculoskeletal Degenerative Diseases DOI Creative Commons
Yili Zheng, Ge Song, Jiabao Guo

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2021, Volume and Issue: 9

Published: Oct. 11, 2021

Musculoskeletal degenerative diseases (MSDDs) are pathological conditions that affect muscle, bone, cartilage, joint and connective tissue, leading to physical functional impairments in patients, mainly consist of osteoarthritis (OA), intervertebral disc degeneration (IDD), rheumatoid arthritis (RA) ankylosing spondylitis (AS). Long non-coding RNAs (lncRNAs) circular (circRNAs) novel regulators gene expression play an important role biological regulation, involving chondrocyte proliferation apoptosis, extracellular matrix degradation peripheral blood mononuclear cell inflammation. Research on MSDD pathogenesis, especially RA AS, is still its infancy major knowledge gaps remain be filled. The effects lncRNA/circRNA-miRNA-mRNA axis progression help us fully understand their contribution the dynamic cellular processes, provide potential OA, IDD, AS therapeutic strategies. Further studies needed explore mutual regulatory mechanisms between lncRNA/circRNA regulation effective interventions pathology MSDD.

Language: Английский

Citations

42

Hair Loss and Telogen Effluvium Related to COVID-19: The Potential Implication of Adipose-Derived Mesenchymal Stem Cells and Platelet-Rich Plasma as Regenerative Strategies DOI Open Access
Pietro Gentile

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(16), P. 9116 - 9116

Published: Aug. 14, 2022

The diffusion of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) inducing disease 2019 (COVID-19) has increased the incidence several dermatological disorders, including hair loss (HL). This article aims to review literature regarding HL and telogen effluvium (TE) in COVID-19 patients critically appraise available evidence role regenerative strategies like Platelet-Rich Plasma (PRP) Human Follicle Stem Cells (HFSCs). A correlation TE analyzing biomolecular pathway involved was performed using PubMed, MEDLINE, Embase, PreMEDLINE, Scopus, Cochrane databases. Observational studies revealed an escalated pattern patients. Psychological stress, systemic inflammation, oxidative stress are potential culprits. Proinflammatory cytokines hormones negatively affect normal metabolism proteoglycans. Reduced anagenic expression proteoglycans is a mediating mechanism that connects COVID-19. Currently, only one study been published on PRP against Further controlled trials required confirm HFSCs efficacy

Language: Английский

Citations

30

The NF-κB Pathway: a Focus on Inflammatory Responses in Spinal Cord Injury DOI
Y. Ding, Qin Chen

Molecular Neurobiology, Journal Year: 2023, Volume and Issue: 60(9), P. 5292 - 5308

Published: June 7, 2023

Language: Английский

Citations

22

LncRNA AC005332.7 Inhibited Ferroptosis to Alleviate Acute Myocardial Infarction Through Regulating miR-331-3p/CCND2 Axis DOI
Rixin Dai, Xiheng Yang, Wujin He

et al.

Korean Circulation Journal, Journal Year: 2023, Volume and Issue: 53(3), P. 151 - 151

Published: Jan. 1, 2023

Acute myocardial infarction (AMI) often occurs suddenly and leads to fatal consequences. Ferroptosis is closely related the progression of AMI. However, specific mechanism ferroptosis in AMI remains unclear.We constructed a cell model using AC16 cells under oxygen glucose deprivation (OGD) conditions mice left anterior descending (LAD) ligation. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide was employed determine viability. levels lactate dehydrogenase, creatine kinase, reactive species (ROS), glutathione (GSH), malondialdehyde (MDA), iron were measured corresponding kits. Dual luciferase reporter gene assay, RNA-binding protein immunoprecipitation, RNA pull-down performed validate correlations among AC005332.7, miR-331-3p, cyclin D2 (CCND2). Hematoxylin eosin staining evaluate damage.AC005332.7 CCND2 lowly expressed, while miR-331-3p highly expressed vivo vitro models AC005332.7 sufficiency reduced ROS, MDA, iron, ACSL4 boosting GSH GPX4, indicating that impeded improve cardiomyocyte injury Mechanistically, interacted with targeted CCND2. Additionally, overexpression or depletion abolished suppressive impact on OGD-induced cells. Moreover, suppressed AMI.AC005332.7 LAD ligation-operated through modulating miR-331-3p/CCND2 axis, thereby mitigating AMI, which proposed novel targets for treatment.

Language: Английский

Citations

18

LncRNA SNHG1 knockdown inhibits hyperglycemia induced ferroptosis viamiR‐16‐5p/ACSL4 axis to alleviate diabetic nephropathy DOI Creative Commons
Xiangdong Fang,

Jianling Song,

Yanxia Chen

et al.

Journal of Diabetes Investigation, Journal Year: 2023, Volume and Issue: 14(9), P. 1056 - 1069

Published: June 14, 2023

Hyperglycemia accelerates the development of diabetic nephropathy (DN) by inducing renal tubular injury. Nevertheless, mechanism has not been elaborated fully. Here, pathogenesis DN was investigated to seek novel treatment strategies.A model established in vivo, levels blood glucose, urine albumin creatinine ratio (ACR), creatinine, urea nitrogen (BUN), malondialdehyde (MDA), glutathione (GSH), and iron were measured. The expression detected qRT-PCR Western blotting. H&E, Masson, PAS staining used assess kidney tissue mitochondria morphology observed transmission electron microscopy (TEM). molecular interaction analyzed using a dual luciferase reporter assay.SNHG1 ACSL4 increased tissues mice, but miR-16-5p decreased. Ferrostatin-1 or SNHG1 knockdown inhibited ferroptosis high glucose (HG)-treated HK-2 cells db/db mice. Subsequently, confirmed be target for SNHG1, directly targeted ACSL4. Overexpression greatly reversed protective roles HG-induced cells.SNHG1 via miR-16-5p/ACSL4 axis alleviate nephropathy, which provided some new insights nephropathy.

Language: Английский

Citations

18