Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

LncRNA X Inactive Specific Transcript Exerts a Protective Effect on High Glucose-Induced Podocytes by Promoting the Podocyte Autophagy via miR-30d-5p/BECN-1 Axis

Cai Y., Chen S., Jiang X., Wu Q., Xu Y., Wang F.

Laboratory Study on Chronic Kidney Disease, published in Int J Endocrinol (2023) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Int J Endocrinol (2023)
Reported sample size
—
Source database
Europe PMC
PMID
36908288
PMCID
PMC10005869
DOI
10.1155/2023/3187846
Citations
10

Abstract (original English)

Inhibiting podocyte autophagy promotes the development of diabetic nephropathy (DN). This study aims to explore the upstream regulatory mechanism of the autophagy-related gene BECN1 in high glucose (HG)-induced podocytes. C57BL/6 mice were treated with 50 mg/kg streptozotocin to construct a DN model. Biochemical indexes, pathological morphology of renal tissue, the morphology of renal podocytes, and the expressions of autophagy-related proteins in DN mice and normal mice were detected. The upstream miRNAs of BECN1 and the upstream long noncoding RNAs (lncRNAs) of miR-30d-5p were predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. Mouse podocyte clone 5 (MPC5) cells were exposed to HG to construct a DN cell model. The levels of miR-30d-5p, X inactive specific transcript (XIST), and BECN1 in mouse kidney and MPC5 cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The regulation of XIST/miR-30d-5p on the viability, apoptosis as well as proteins related to apoptosis, epithelial-mesenchymal transition (EMT), and autophagy in MPC5 cells were determined by rescue experiments. The levels of glucose, urinary protein, serum creatinine, and blood urea nitrogen were upregulated, but the kidney tissues and podocytes were damaged in DN mice. XIST targeted miR-30d-5p to promote viability while suppressing the apoptosis of HG-ind

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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