Evidence map›Paper›PMID 38965127›Full record

ArticleMolecular and cellular biochemistry2025

Tirzepatide alleviates oxidative stress and inflammation in diabetic nephropathy via IL-17 signaling pathway.

Yong Yang, Yiyong Wang, Yong Zhou, Jing Deng, Lihao Wu

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
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  5. The role of the incretin GIP in inflammation.Journal of endocrinological investigation · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Revolutionizing type 2 diabetes management: the role of the pharmacist in unlocking the potential of tirzepatide.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025
    Review
  11. Review
  12. Article
  13. Review
  14. Review
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  16. Article
  17. Article
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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

5 authors.

Yong YangDivision of Cardiac Arrhythmia, Cardiac and Vascular Center, The University of Hong Kong-Shenzhen Hospital, Haiyuan 1st Road, Shenzhen, Guangdong, China. yongyang_yyang@163.com.
Yiyong WangDepartment of Cardiovascular Medicine, General Hospital of Ningxia Medical University, No. 804 Shengli South Street, Yinchuan, Ningxia, China.
Yong ZhouDepartment of Oncology, Shenzhen Hospital of Southern Medical University, No. 1333 Xinhu Road, Shenzhen, Guangdong, China.
Jing DengDepartment of Cardiovascular Internal Medicine, Shenzhen Hospital of Southern Medical University, No. 1333 Xinhu Road, Shenzhen, 518053, Guangdong, China.
Lihao WuDepartment of Cardiovascular Medicine, University of Chinese Academy of Science Shenzhen Hospital, No. 4253 Matian Street, Shenzhen, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress (OS) and inflammation play essential roles in the development of diabetic nephropathy (DN). Tirzepatide (TZP) has a protective effect in diabetes. However, its underlying mechanism in DN remains unclear. DN model mice were induced by intraperitoneal injection of streptozotocin (STZ; 60 mg/kg), followed by administration of different doses of TZP (3 and 10 nmol/kg) via intraperitoneal injection for 8 weeks. The effects of TZP on DN were evaluated by detecting DN-related biochemical indicators, kidney histopathology, apoptosis, OS, and inflammation levels. Additionally, to further reveal the potential mechanism, we investigated the role of TZP in modulating the IL-17 pathway. TZP reduced serum creatinine (sCR), blood urea nitrogen (BUN), and advanced glycosylation end products (AGEs) levels, while simultaneously promoting insulin secretion in diabetic mice. Additionally, TZP attenuated tubular and glomerular injury and reduced renal apoptosis levels. Further studies found that TZP increased the levels of SOD and CAT, and decreased MDA. Meanwhile, TZP also reduced the expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in both mouse serum and kidney homogenates. TZP effectively inhibited the IL-17 pathway, and subsequent intervention with an IL-17 pathway agonist (IL-17A) reversed the suppressive effects of TZP on OS and inflammation. TZP can improve DN by inhibiting OS and inflammation through the suppression of the IL-17 pathway.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic NephropathiesInflammationInterleukin-17Oxidative StressSignal TransductionAnimalsMaleMiceTirzepatideIl17a protein, mouseInterleukin-17TirzepatideDiabetic nephropathyIL-17 pathwayInflammationOxidative stressTirzepatide

Identifiers

PMID38965127

What OpenQuestion holds

Texttitle and abstract
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Registered trials

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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.