ArticleCell death discovery2023
Tim-3 protects against cisplatin nephrotoxicity by inhibiting NF-κB-mediated inflammation.
Article in Cell death discovery, 2023. 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 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Silencing of HAVCR2 Attenuates Skeletal Muscle Ischemia-Reperfusion Injury by Inhibiting Oxidative Stress.Biochemical genetics · 2026Article
- T-Cell Remodeling in Renal Fibrosis: From Acute Injury to Chronic Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Galaxamide Ameliorates Cisplatin-induced Uterine Injury via Anti‑inflammatory and Antiapoptotic Mechanisms in Mice.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Unlocking the roles of plasma soluble T-cell immunoglobulin and mucin domain-containing protein 3 in kidney diseases: findings from native and allograft biopsy cohorts.Molecular biomedicine · 2026Article
- TIM-3, a potential target for sepsis therapy.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026Review
- Paeonol protects against cisplatin-induced premature ovarian failure via anti-inflammatory and antioxidant activities: an integrated approach of network pharmacology, molecular dynamics simulation, and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- TRPV1 blockade restores the baroreflex control of renal sympathetic nerve activity in cisplatin-induced renal injury in rats.Experimental physiology · 2025Article
- Design, Synthesis, and Evaluation of New 2-Arylpropanoic Acid-l-Tryptophan Derivatives for Mitigating Cisplatin-Induced Nephrotoxicity.Molecules (Basel, Switzerland) · 2025Article
- Tim-3 Deficiency Ameliorates Motor Deficits and Neuroinflammation in MPP+/MPTP-Induced Parkinson's Disease Models via the NF-κB/NLRP3 Pathway.Molecular neurobiology · 2025Article
- Protocatechuic Acid Ameliorates Cisplatin-Induced Inflammation and Apoptosis in Mouse Proximal Tubular Cells.International journal of molecular sciences · 2025Article
- Attenuation of cisplatin-induced acute kidney injury by sanguinarine: modulation of oxidative stress, inflammation, and cellular damage.Frontiers in pharmacology · 2025Article
- Time-restricted feeding protects against cisplatin-induced acute kidney injury in mice.Kidney research and clinical practice · 2024Article
- The cross-talk between macrophages and tumor cells as a target for cancer treatment.Frontiers in oncology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The impact of Tim-3 (T cell immunoglobulin and mucin domain-containing protein 3) on cisplatin-induced acute kidney injury was investigated in this study. Cisplatin-induced Tim-3 expression in mice kidney tissues and proximal tubule-derived BUMPT cells in a time-dependent manner. Compared with wild-type mice, Tim-3 knockout mice have higher levels of serum creatinine and urea nitrogen, enhanced TUNEL staining signals, more severe 8-OHdG (8-hydroxy-2' -deoxyguanosine) accumulation, and increased cleavage of caspase 3. The purified soluble Tim-3 (sTim-3) protein was used to intervene in cisplatin-stimulated BUMPT cells by competitively binding to the Tim-3 ligand. sTim-3 obviously increased the cisplatin-induced cell apoptosis. Under cisplatin treatment conditions, Tim-3 knockout or sTim-3 promoted the expression of TNF-α (tumor necrosis factor-alpha) and IL-1β (Interleukin-1 beta) and inhibited the expression of IL-10 (interleukin-10). NF-κB (nuclear factor kappa light chain enhancer of activated B cells) P65 inhibitor PDTC or TPCA1 lowed the increased levels of creatinine and BUN (blood urea nitrogen) in cisplatin-treated Tim-3 knockout mice serum and the increased cleavage of caspase 3 in sTim-3 and cisplatin-treated BUMPT cells. Moreover, sTim-3 enhanced mitochondrial oxidative stress in cisplatin-induced BUMPT cells, which can be mitigated by PDTC. These data indicate that Tim-3 may protect against renal injury by inhibiting NF-κB-mediated inflammation and oxidative stress.
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.