Evidence map›Paper›PMID 38326870›Full record

ArticleDiabetology & metabolic syndrome2024

Dapagliflozin improves podocytes injury in diabetic nephropathy via regulating cholesterol balance through KLF5 targeting the ABCA1 signalling pathway.

Jingshu Sun, Xinyu Zhang, Simeng Wang, Dandan Chen, Jianqiang Shu, Nannan Chong, Qinglian Wang, Ying Xu

Abstract read
In one paragraph

Article in Diabetology & metabolic syndrome, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
–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

12 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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

8 authors.

Jingshu Sun *Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Xinyu Zhang *Shandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Simeng WangShandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Dandan ChenShandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Jianqiang ShuShandong Provincial Hospital, Shandong University, Jinan, Shandong, China.
Nannan ChongDepartment of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Qinglian WangShandong Provincial Hospital, Shandong University, Jinan, Shandong, China. 15216401100@163.com.
Ying XuShandong Provincial Hospital, Shandong University, Jinan, Shandong, China. 15562450030@163.com.

Funding

National Natural Science Foundation of China 81500553Natural Science Foundation of Shandong Province ZR2021QH137
6 · The paper itself

Abstract

Diabetic nephropathy (DN), one of the more prevalent microvascular complications in patients diagnosed with diabetes mellitus, is attributed as the main cause of end-stage renal disease (ESRD). Lipotoxicity in podocytes caused by hyperglycemia has been recognised as a significant pathology change, resulting in the deterioration of the glomerular filtration barrier. Research has demonstrated how dapagliflozin, a kind of SGLT2i, exhibits a multifaceted and powerful protective effect in DN, entirely independent of the hypoglycemic effect, with the specific mechanism verified. In this present study, we found that dapagliflozin has the potential to alleviate apoptosis and restore cytoskeleton triggered by high glucose (HG) in vivo and in vitro. We also discovered that dapagliflozin could mitigate podocyte cholesterol accumulation by restoring the expression of ABCA1, which is the key pathway for cholesterol outflows. This research also mechanistically demonstrates that the protective effect of dapagliflozin can be mediated by KLF-5, which is the upstream transcription factor of ABCA1. Taken together, our data suggest that dapagliflozin offers significant potential in alleviating podocyte injury and cholesterol accumulation triggered by high glucose. In terms of the mechanism, we herein reveal that dapagliflozin could accelerate cholesterol efflux by restoring the expression of ABCA1, which is directly regulated by KLF-5.

Indexed as

ABCA1CholesterolDapagliflozinDiabetic NephropathyKLF-5

Identifiers

PMID38326870
PMCPMC10851504

What Socratic holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

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.