Evidence mapPaperPMID 37446016Full record

ArticleInternational journal of molecular sciences2023

Accumulation of Renal Fibrosis in Hyperuricemia Rats Is Attributed to the Recruitment of Mast Cells, Activation of the TGF-β1/Smad2/3 Pathway, and Aggravation of Oxidative Stress.

Mingkang Zhang, Ruirui Cui, Yan Zhou, Yanrong Ma, Yongwen Jin, Lina Wang, Wen Kou, Xin'an Wu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
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

6 citing papers in PubMed, 11 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Mingkang ZhangSchool of Pharmacy, Lanzhou University, Lanzhou 730000, China.
Ruirui CuiSchool of Pharmacy, Lanzhou University, Lanzhou 730000, China.
Yan ZhouEngineering Research Centre of Prevention and Control for Clinical Medication Risk, Lanzhou 730000, China.
Yanrong MaSchool of Pharmacy, Lanzhou University, Lanzhou 730000, China.
Yongwen JinSchool of Pharmacy, Lanzhou University, Lanzhou 730000, China.
Lina WangDepartment of Pharmacy, The First Hospital of Lanzhou University, Lanzhou 730000, China.
Wen KouEngineering Research Centre of Prevention and Control for Clinical Medication Risk, Lanzhou 730000, China.
Xin'an WuSchool of Pharmacy, Lanzhou University, Lanzhou 730000, China.ORCID 0000-0002-0371-0361
First Hospital of Lanzhou University · CNLanzhou University · CN

Funding

the First Hospital of Lanzhou University intramural fund ldyyyn2019-30 and ldyyyn2022-89the National Natural Science Foundation of China 82060676, 81960680, U21A20424the Natural Science Foundation of Gansu No. 21ZD4FA014the Science and Technology Planning Project of Chengguan District, Lanzhou City 2019RCCX0039
6 · The paper itself

Abstract

Renal fibrosis is relentlessly progressive and irreversible, and a life-threatening risk. With the continuous intake of a high-purine diet, hyperuricemia has become a health risk factor in addition to hyperglycemia, hypertension, and hyperlipidemia. Hyperuricemia is also an independent risk factor for renal interstitial fibrosis. Numerous studies have reported that increased mast cells (MCs) are closely associated with kidney injury induced by different triggering factors. This study investigated the effect of MCs on renal injury in rats caused by hyperuricemia and the relationship between MCs and renal fibrosis. Our results reveal that hyperuricemia contributes to renal injury, with a significant increase in renal MCs, leading to renal fibrosis, mitochondrial structural disorders, and oxidative stress damage. The administration of the MCs membrane stabilizer, sodium cromoglycate (SCG), decreased the expression of SCF/c-kit, reduced the expression of α-SMA, MMP2, and inhibited the TGF-β1/Smad2/3 pathway, thereby alleviating renal fibrosis. Additionally, SCG reduced renal oxidative stress and mitigated mitochondrial structural damage by inhibiting Ang II production and increasing renal GSH, GSH-Px, and GR levels. Collectively, the recruitment of MCs, activation of the TGF-β1/Smad2/3 pathway, and Ang II production drive renal oxidative stress, ultimately promoting the progression of renal fibrosis in hyperuricemic rats.

Indexed as

HyperuricemiaKidney DiseasesAnimalsFibrosisKidneyMast CellsOxidative StressRatsSignal TransductionTransforming Growth Factor beta1Transforming Growth Factor beta1hyperuricemiamast cellsoxidative stressrenal fibrosisTGF-β1/Smad2/3 pathway

Identifiers

PMID37446016
PMCPMC10341566
OpenAlexW4382787543

What Socratic holds

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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.