ArticleRedox biology2022
Upregulation of TIPE1 in tubular epithelial cell aggravates diabetic nephropathy by disrupting PHB2 mediated mitophagy.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 103 citations in OpenAlex.
- ADAMTS13 ameliorates diabetic nephropathy by Nrf2/GPX4/eNOS signaling pathway.Renal failure · 2026Article
- Imbalance of mitochondria and abnormalities in lipid metabolism in Diabetic Tubulopathy.Annals of medicine · 2026Review
- Targeting mitochondrial quality control in diabetic kidney disease: emerging therapeutic opportunities.Renal failure · 2026Review
- Mitochondrial dysfunction drives metabolic reprogramming in Gitelman syndrome: insights from proteomics and isogenic modeling.Human genetics · 2026Article
- Compensatory Mitophagy via NEDD4/HIF-1α/BNIP3 Pathway Restrains EndMT and Renal Allograft Interstitial Fibrosis Induced by TNFα.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The deubiquitinase YOD1 in renal tubular epithelial cells promotes diabetic kidney disease by stabilizing KEAP1.Acta pharmacologica Sinica · 2026Article
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- FOSL1 upregulation contributes to ischemia/reperfusion-induced acute kidney injury by regulating GPX4-dependent ferroptosis.Biology direct · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Targeting posttranslational modifications of oxidative stress pathways for the treatment of diabetic nephropathy.Journal of pharmaceutical analysis · 2026Review
- Leocarpinolide B alleviates epithelial tubular mitochondrial dysfunction via macrophage exosomal miR-204-5p/TFAM axis in AKI-CKD transition.Journal of nanobiotechnology · 2026Article
- SIRT1-regulated mitophagy mitigates lipotoxicity-induced ferroptosis in diabetic kidney disease.Apoptosis : an international journal on programmed cell death · 2026Article
- DYRK2 drives renal fibrosis through CDK1-dependent G2/M phase dysregulation in tubular epithelial cells.Cellular & molecular biology letters · 2026Article
- Macrophage TRIM21 Inhibition Ameliorates Murine Acute Pancreatitis via PHB2-Mediated Mitochondrial Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Upregulation of PPTC7 in brain microvascular endothelial cell aggravates diabetic cognitive dysfunction by impairing PHB2 mediated mitochondrial function.Redox biology · 2026Article
- Integrated Transcriptomic Analysis Identifies TAP1 as a Key Regulator of PANoptosis in Diabetic Kidney Disease Tubular Injury.Inflammation · 2026Article
- PACS-2 Mitigates NPSC Apoptosis and Intervertebral Disc Degeneration by Preserving MAM Integrity via the SP1/LRRK2/Mfn2 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitophagy and Cellular Homeostasis in Kidney Diseases: Mechanisms and Potential Therapeutics.International journal of biological sciences · 2026Review
- Focusing on the Apolipoprotein M-Mitophagy Axis: A Mechanism for Renal Protection in Diabetic Nephropathy.Journal of diabetes research · 2026Review
- Dual Phosphorylation of STAT1 at Y701/S727 by TNFα Drives AIM2-Mediated PANoptosis of Renal Tubular Epithelial Cells and Fibrotic Progression in Renal Allografts.International journal of biological sciences · 2026Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal tubular epithelial cells (RTECs) are one of the most mitochondria-rich cell types, and are thus vulnerable to mitochondrial dysregulation, which is defined as a pivotal event in tubular damage in diabetic nephropathy (DN). However, the underlying mechanisms remain largely unknown. Here, we investigated the role and mechanisms of tumor necrosis factor alpha-induced protein 8-like 1 (TNFAIP8L1/TIPE1) in high glucose (HG)-induced mitochondrial dysfunction in RTECs and DN progression. TIPE1 expression was predominantly upregulated in RTECs in patients with DN and mice with streptozotocin (STZ)-induced DN. Conditional knockout of Tipe1 in RTECs significantly decreased the urine protein creatinine ratio, renal tubular damage, epithelial-mesenchymal transition, and interstitial fibrosis in STZ-induced mice. RNA sequencing revealed that citrate cycle-related genes were positively enriched in the renal tissues of RTEC-specific Tipe1 knockout mice. Tipe1 deficiency upregulated ATP levels, mitochondrial membrane potential, and respiration rate, but downregulated mitochondrial ROS levels in RTECs. Furthermore, Tipe1 ablation led to enhanced mitophagy in RTECs, indicative of increased LC3II, PINK1, and Parkin expression, but decreased p62 expression in mitochondria. Mechanistically, mass spectrometry screening and co-immunoprecipitation assays revealed the interaction of TIPE1 with prohibitin 2 (PHB2), a crucial mitophagy receptor. Intriguingly, TIPE1 promoted the ubiquitination and proteasomal degradation of PHB2. Subsequently, PHB2 knockdown almost abrogated the improvement of Tipe1 loss on HG-induced tubular cell mitophagy and damage. Thus, TIPE1 disrupts mitochondrial homeostasis in RTECs and promotes tubular damage by destabilizing PHB2 under HG conditions. Hence, TIPE1 may act as a potential therapeutic target to prevent DN progression.
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