Evidence map›Paper›PMID 39082470›Full record

ArticleRenal failure2024

Sirt6 overexpression relieves ferroptosis and delays the progression of diabetic nephropathy via Nrf2/GPX4 pathway.

Lingyu Du, Canghui Guo, Shengnan Zeng, Ke Yu, Maodong Liu, Ying Li

Abstract read
In one paragraph

Article in Renal failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed.

  1. Review
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  9. Frontiers in pharmacology · 2026
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  16. SIRT6 inhibits endoplasmic reticulum stress-mediated ferroptosis by activating Nrf2/HO-1 signaling to alleviate osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  17. Article
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  19. [Roles of ferroptosis in the development of diabetic nephropathy].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Lingyu DuDepartment of Nephrology, Hebei Medical University Third Hospital, Shijiazhuang City, Hebei Province, China.
Canghui GuoDepartment of Nephrology, Hebei Medical University Third Hospital, Shijiazhuang City, Hebei Province, China.
Shengnan ZengDepartment of Nephrology, Hebei Medical University Third Hospital, Shijiazhuang City, Hebei Province, China.
Ke YuDepartment of Nephrology, Hebei Medical University Third Hospital, Shijiazhuang City, Hebei Province, China.
Maodong LiuDepartment of Nephrology, Hebei Medical University Third Hospital, Shijiazhuang City, Hebei Province, China.
Ying LiDepartment of Nephrology, Hebei Medical University Third Hospital, Shijiazhuang City, Hebei Province, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSirt6, reactive oxygen species and ferroptosis may participate in the pathogenesis of Diabetic Nephropathy (DN). Exploring the relationship between Sirt6, oxidative stress, and ferroptosis provides new scientific ideas to DN.

methodsHuman podocytes were stimulated with 30 mM glucose and 5.5 mM glucose. The mice of db/db group were randomly divided into two groups:12 weeks and 16 weeks. Collect mouse blood and urine specimens and renal cortices for investigations. HE, Masson, PAS and immunohistochemical staining were used to observe pathological changes. Western blot, RT-qPCR and immunofluorescence staining were used to evaluate expression of relevant molecules. CCK8 method was introduced to observe cell viability. The changes of podocyte mitochondrial membrane potential and mitochondrial morphology in each group were determined by JC-1 staining and Mito-Tracker.

resultsThe expression level of Sirt6, Nrf2, SLC7A11, HO1, SOD2 and GPX4 were reduced, while ACSL4 was increased in DN. Blood glucose, BUN, Scr, TG, T-CHO and 24h urine protein were upregulated, while ALB was reduced in diabetic group. The treatment of Ferrostatin-1 significantly improved these changes, which proved ferroptosis was involved in the development of DN. Overexpression of Sirt6 might ameliorate the oxidation irritable reaction and ferroptosis. Sirt6 plasmid transfection increased mitochondrial membrane potential and protected morphology and structure of mitochondria. The application of Sirt6 siRNA could aggravated the damage manifestations.

conclusionHigh glucose stimulation could decrease the antioxidant capacity and increase formation of ROS and lipid peroxidation. Sirt6 might alleviate HG-induced mitochondrial dysfunction, podocyte injury and ferroptosis through regulating Nrf2/GPX4 pathway.

Indexed as

Diabetic NephropathiesFerroptosisNF-E2-Related Factor 2Phospholipid Hydroperoxide Glutathione PeroxidasePodocytesSirtuinsAnimalsDisease ProgressionHumansMaleMiceOxidative StressReactive Oxygen SpeciesSignal Transductionglutathione peroxidase 4, mouseNFE2L2 protein, humanNfe2l2 protein, mouseNF-E2-Related Factor 2Phospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesSIRT6 protein, humanSirt6 protein, mouseSirtuinsDiabetic nephropathyferroptosismitochondrial dysfunctionpodocytesSirt6

Identifiers

PMID39082470
PMCPMC11293269

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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 OpenQuestion graph.