Evidence map›Paper›PMID 39754634›Full record

ArticleJournal of bioenergetics and biomembranes2025

Sirt6 regulates the Notch signaling pathway and mediates autophagy and regulates podocyte damage in diabetic nephropathy.

Ping Ma, Hailin Shao, Donghong Xu, Xiaoyu Qi

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Article in Journal of bioenergetics and biomembranes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Ping MaDepartment of Endocrinology, Tianjin 4th Center Hospital, Tianjin, 300140, China. mp87560@163.com.
Hailin ShaoDepartment of Endocrinology, Tianjin 4th Center Hospital, Tianjin, 300140, China.
Donghong XuDepartment of Endocrinology, Tianjin 4th Center Hospital, Tianjin, 300140, China.
Xiaoyu QiDepartment of Endocrinology, Tianjin 4th Center Hospital, Tianjin, 300140, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate the role of silent information regulator 6 (SIRT6) in regulating podocyte injury in diabetic nephropathy (DN) through autophagy mediated by Notch signaling pathway. A blank control group (group A), a diabetic nephropathy group (group B), and a Sirt6 intervention group (group C) were established. The group A cells were human normal glomerular podocyte cell lines (HGPCs) without any treatment. In group B, the cells were cultivated in glucose medium containing 30 mmol/L and a 10 µmol/L anti-LSirt6 antibody solution. Three sets of cells were tested for their capacity to proliferate via CCK8, for protein expression via Western blot, for associated mRNA expression levels via qPCR, and for cell migration and invasion ability via Transwell. The podocyte proliferation and migration activity in group B were reduced compared to group A, while these properties in group C were elevated compared to group B (DN). B Group is diabetes nephropathy. Compared with those in group B, the number of invading podocytes in group C were greater than those in group A, and the overall apoptosis rate in group C was lower than that in group B. The expression levels of apoptotic proteins in the podocytes in group C were greater than those in group B, and the bcl-2 level was lower than those in group B. The Notch1 and Jagged1 mRNA and protein levels in the podocytes in group B were greater than those in group A, whereas those in the podocytes in group C were lower than those in group B. Sirt6 can protect against podocyte autophagy injury in DN by regulating the Notch1 signaling pathway.

Indexed as

AutophagyDiabetic NephropathiesPodocytesReceptors, NotchSirtuinsApoptosisHumansSignal TransductionReceptors, NotchSIRT6 protein, humanSirtuinsAutophagyDiabetes nephropathyInformation regulatory factor 6NotchPodocyte

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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.