Evidence mapPaperPMID 39194535Full record

ArticleBiology2024

Schisandrin A Attenuates Diabetic Nephropathy via EGFR/AKT/GSK3β Signaling Pathway Based on Network Pharmacology and Experimental Validation.

Pengyu Wang, Qing Lan, Qi Huang, Ruyi Zhang, Shuo Zhang, Leiming Yang, Yan Song, Tong Wang, Guandi Ma, Xiufen Liu and 3 more

Abstract read
In one paragraph

Article in Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Discovery of vasodilatory effects of NaActa pharmacologica Sinica · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
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

13 authors.

Pengyu WangSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Qing LanSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Qi HuangSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Ruyi ZhangSchool of Pharmacy, Hubei University of Chinese Medicine, Wuhan 430000, China.ORCID 0000-0001-6469-998X
Shuo ZhangSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Leiming YangSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Yan SongSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Tong WangSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Guandi MaSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Xiufen LiuHubei Key Laboratory of Diabetes and Angiopathy, Medical Research Institute, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Xiying GuoHubei Key Laboratory of Diabetes and Angiopathy, Medical Research Institute, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.ORCID 0000-0002-6317-6279
Youzhi ZhangSchool of Pharmacy, Hubei Engineering Research Center of Traditional Chinese Medicine of South Hubei Province, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.
Chao LiuHubei Key Laboratory of Diabetes and Angiopathy, Medical Research Institute, Xianning Medical College, Hubei University of Science and Technology, Xianning 437100, China.

Funding

Hubei Key Laboratory of Diabetes and Angiopathy Program of Hubei University of Science and Technology 2020XZ10Hubei University of Science and Technology School-level Fund BK202027, 2022TNB01, 2024TNB02Project of Education Commission of Hubei Province B2022192, D20202802Provincial Science and Technology Plan Project Funds of Hubei Province 2021DFE025
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is one of the common complications of diabetes and the main cause of end-stage renal disease (ESRD) in clinical practice. Schisandrin A (Sch A) has multiple pharmacological activities, including inhibiting fibrosis, reducing apoptosis and oxidative stress, and regulating immunity, but its pharmacological mechanism for the treatment of DN is still unclear. In vivo, streptozotocin (STZ) and a high-fat diet were used to induce type 2 diabetic rats, and Sch A was administered for 4 weeks. At the same time, protein-protein interaction (PPI) networks were established to analyze the overlapping genes of DN and Sch A. Subsequently, the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to determine the hub pathway. In addition, molecular docking was used to preliminarily verify the affinity of hub proteins and Sch A. Further, H&E staining, Sirius red staining, immunohistochemistry, immunofluorescence, and western blot analysis were used to detect the location and expression of related proteins in DN. This study revealed the multi-target and multi-pathway characteristics of Sch A in the treatment of DN. First, Sch A could effectively improve glucose tolerance, reduce urine microprotein and urine creatinine levels, and alleviate renal pathological damage in DN rats. Second, EGFR was the hub gene screened in overlapping genes (43) of Sch A (100) and DN (2524). Finally, it was revealed that Sch A could inhibit the protein expression levels of EGFR and PTRF and reduced the expression of apoptosis-related proteins, and this effect was related to the modulation of the AKT/GSK-3β signaling pathway. In summary, Sch A has a protective effect in DN rats, EGFR may be a potential therapeutic target, throughout modulating AKT/GSK-3β pathway.

Indexed as

AKT/GSK-3βdiabetic nephropathyEGFRnetwork pharmacologyratSchisandrin A

Identifiers

PMID39194535
PMCPMC11351691

What Socratic holds

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LicenceCC BY
Read underepoch 390

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.