ArticleCell death & disease2024
LncRNA PVT1 induces mitochondrial dysfunction of podocytes via TRIM56 in diabetic kidney disease.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Approach to Studies on Podocyte Lesions Mediated by Hyperglycemia: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Serum long noncoding RNA human plasmacytoma variant translocation 1 (PVT1) expression levels in Egyptians type 2 diabetic patients and its correlation with severity of diabetic nephropathy.BMC endocrine disorders · 2026Article
- The versatile roles of long non-coding RNAs in kidney disease.Nature reviews. Nephrology · 2026Review
- Targeting the lncRNA PVT-1-Hippo signaling axis in kidney diseases: an emerging therapeutic paradigm.Molecular biology reports · 2026Review
- Long Noncoding RNA PCALRx Interacts with Pyruvate Carboxylase to Drive Multi-Organ Developmental Toxicity in Zebrafish Embryos Exposed to Amoxicillin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Article
- From mechanisms to therapies: exploiting epigenetic and post-translational modifications of mitochondrial quality control in diabetic kidney disease.Frontiers in endocrinology · 2026Review
- Diabetic kidney disease: exploring mechanistic depths and the future of pharmacological intervention.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Review
- Mitochondrial quality control in diabetes mellitus and complications: molecular mechanisms and therapeutic strategies.Cell death & disease · 2025Review
- Inhibition of miR-615-3p enhances dentinogenesis in scapStem cell research & therapy · 2025Article
- The association between diabetes and head and neck squamous cell carcinoma: evidence from clinical cohort and bioinformatics analyses.Frontiers in genetics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
Mitochondrial dysfunction is a significant contributor to podocyte injury in diabetic kidney disease (DKD). While previous studies have shown that PVT1 might play a vital role in DKD, the precise molecular mechanisms are largely unknown. By analyzing the plasma and kidney tissues of DKD patients, we observed a significant upregulation of PVT1 expression, which exhibited a positive correlation with albumin/creatinine ratios and serum creatinine levels. Then, we generated mice with podocyte-specific deletion of PVT1 (Nphs2-Cre/Pvt1
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.