ArticleRedox report : communications in free radical research2024
WTAP-mediated m
Article in Redox report : communications in free radical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Targeting mitochondrial quality control in diabetic kidney disease: emerging therapeutic opportunities.Renal failure · 2026Review
- Ubiquitination plays a key role in an insecticide resistance fitness cost.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Ubiquitination-Related Diagnostic Biomarkers for Diabetic Nephropathy: Insights From Multiomic Analysis, Drug Docking, and Experimental Validation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Targeting posttranslational modifications of oxidative stress pathways for the treatment of diabetic nephropathy.Journal of pharmaceutical analysis · 2026Review
- The Role of NMedComm · 2026Review
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- From mechanisms to therapies: exploiting epigenetic and post-translational modifications of mitochondrial quality control in diabetic kidney disease.Frontiers in endocrinology · 2026Review
- The TRIM14-KIF1B Axis Drives Renal Injury in Diabetic Nephropathy Through TLR4/NF-κB Pathway Modulation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Role of metabolic reprogramming and lactylation in diabetic nephropathy: molecular mechanisms and therapeutic prospects - a narrative review.Frontiers in endocrinology · 2026Review
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Smurf2 knockdown attenuates the progression of diabetic nephropathy by inhibiting mesangial cell proliferation and fibrosis through suppressing EYA2 ubiquitination.Renal failure · 2025Article
- Mitochondrial quality control in diabetes mellitus and complications: molecular mechanisms and therapeutic strategies.Cell death & disease · 2025Review
- Tanshinone IIA suppresses the proliferation and fibrosis of mesangial cell in diabetic nephropathy though WTAP-mediated mScientific reports · 2025Article
- The latest progression of N6-methyladenosine (mFrontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesDiabetic nephropathy (DN) is one of the most serious microvascular complications of diabetes and is the most common cause of end-stage renal disease. Tripartite motif-containing (TRIM) proteins are a large family of E3 ubiquitin ligases that contribute to protein quality control by regulating the ubiquitin - proteasome system. However, the detailed mechanisms through which various TRIM proteins regulate downstream events have not yet been fully elucidated. The current research aimed to determine the function and mechanism of TRIM22 in DN.
methodsDN models were established by inducing HK-2 cells using high glucose (HG) and diabetic mice (db/db mice). Cell viability, apoptosis, mitochondrial reactive oxygen species, and mitochondrial membrane potential were detected by Cell Counting Kit-8 and flow cytometry, respectively. Pathological changes were evaluated using hematoxylin and eosin, periodic acid schiff and Masson staining. The binding between TRIM22 and optic atrophy 1 (OPA1) was analyzed using co-immunoprecipitation. The m
resultsTRIM22 was highly expressed in patients with DN. TRIM22 silencing inhibited HG-induced apoptosis and mitochondrial dysfunction in HK-2 cells. Promoting mitochondrial fusion alleviated TRIM22 overexpression-induced cell apoptosis, mitochondrial dysfunction in HK-2 cells, and kidney damage in mice. Mechanistically, TRIM22 interacted with OPA1 and induced its ubiquitination. Wilms tumor 1-associating protein (WTAP) promoted m DISCUSSION: TRIM22 silencing inhibited the progression of DN by interacting with OPA1 and inducing its ubiquitination. Furthermore, WTAP promoted m
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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 Socratic graph.