ArticleClinical and experimental nephrology2021
MiR-142-3p ameliorates high glucose-induced renal tubular epithelial cell injury by targeting BOD1.
Article in Clinical and experimental nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- A Pilot Study of Circulating microRNA Expression in Newly Diagnosed Type 2 Diabetes Using a Pooled Sample Approach.Clinics and practice · 2026Article
- LncRNA SNHG7/miR-181b-5p/TLR4 Activates Inflammation And Promotes Pyroptosis Through NF-κB Signaling in Diabetic Nephropathy.Inflammation · 2025Article
- Expression and diagnostic value evaluation of urinary exosomal miR-142-3p in diabetic nephropathy.Scientific reports · 2025Article
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- miRNA-142-3p aggravates hydrogen peroxide-induced human umbilical vein endothelial cell premature senescence by targeting SIRT1.Bioscience reports · 2024Article
- The Expression of miR-377-3p in Patients with DKD and the Regulatory Mechanism of miR-377-3p on the Inflammatory Response of HK-2 Cells Through TGF-β.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Broadening horizons: the contribution of mitochondria-associated endoplasmic reticulum membrane (MAM) dysfunction in diabetic kidney disease.International journal of biological sciences · 2023Review
- MicroRNA-122-5p ameliorates tubular injury in diabetic nephropathy via FIH-1/HIF-1α pathway.Renal failure · 2022Article
- Circulating miRNA as potential biomarkers for diabetes mellitus type 2: should we focus on searching for sex differences?Journal of applied genetics · 2022Review
- Cellular mechanism of action of forsythiaside for the treatment of diabetic kidney disease.Frontiers in pharmacology · 2022Article
- Identification of Genes Reveals the Mechanism of Cell Ferroptosis in Diabetic Nephropathy.Frontiers in physiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTubular injury plays a crucial role in the pathogenesis of diabetic nephropathy (DN). It is well known that many microRNAs (miRNAs) exert crucial effects on tubular injury. This study intends to explore the effect of miR-142-3p on the apoptosis and oxidative stress of high glucose (HG)-treated renal tubular epithelial cells (HK-2) and its underlying mechanism. MATERIALS AND
methodsHK-2 cells were exposed to HG to mimic cell injury. MTT assays and flow cytometry analyses were conducted to measure cell viability and cell apoptosis, respectively. RT-qPCR and western blot analyses were carried out to detect RNA and protein levels, respectively. The levels of oxidative stress markers were evaluated by ELISA. The binding between miR-142-3p and biorientation of chromosomes in cell division 1 (BOD1) was validated by a luciferase reporter assay.
resultMiR-142-3p is low-expressed in HG-stimulated HK-2 cells. Functionally, miR-142-3p overexpression attenuates the apoptosis and oxidative stress of HG-stimulated HK-2 cells. Mechanistically, BOD1 was confirmed to be targeted by miR-142-3p in HK-2 cells. Moreover, BOD1 overexpression reversed the suppressive effect of miR-142-3p overexpression on the apoptosis and oxidative stress of HK-2 cells treated with HG.
conclusionMiR-142-3p ameliorates HG-induced renal tubular epithelial cell injury by targeting BOD1. The finding might provide novel insight into the role of miR-142-3p/BOD1 axis in DN treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.