Evidence map›Paper›PMID 35433764›Full record

ArticleFrontiers in medicine2022

SUMO1 Promotes Mesangial Cell Proliferation Through Inhibiting Autophagy in a Cell Model of IgA Nephropathy.

Xia Tan, Yexin Liu, Di Liu, Xiaofang Tang, Ming Xia, Guochun Chen, Liyu He, Xuejing Zhu, Hong Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in medicine, 2022. 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
0.6field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
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

9 authors at 2 institutions in 1 country.

Xia TanDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Yexin LiuDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Di LiuDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Xiaofang TangDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Ming XiaDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Guochun ChenDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Liyu HeDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Xuejing ZhuDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Hong LiuDepartment of Nephrology, Key Lab of Kidney Disease and Blood Purification in Hunan, The Second Xiangya Hospital of Central South University, Renal Research Institute of Central South University, Changsha, China.
Central South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA nephropathy (IgAN) is a common form of primary glomerulonephritis and its main pathological changes are mesangial cell proliferation and matrix expansion. Autophagy inhibition may result in its mesangial cell proliferation and renal lesions. SUMOylation is a eukaryotic-reversible post-translational modification where SUMO is covalently attached to target proteins to regulate their properties. It is largely unclear whether SUMOylation contributes to the pathogenesis of IgAN. This study was designed to investigate the change of protein SUMO1 in mesangial cells of IgAN and its association with autophagy. We found the expression of SUMO1 was upregulated in IgAN, IgA mouse model, and aIgA1-stimulated mesangial cells. In aIgA1-stimulated mesangial cell model, we tested LC3II/I and p62, the autophagy-related proteins suggested the inhibition of autophagy. Inhibited SUMOylation with ginkgolic acid (GA) or silencing SUMO1 could downregulate SUMO1 and SUMO1-p53, promote autophagy, and lessen cell proliferation. In summary, in the mesangial cells stimulated with aIgA1, SUMO1 may contribute to its cell proliferation through inhibited autophagy, and SUMO1-p53 may play a role in this process.

Indexed as

autophagyIgA nephropathymesangial cellproliferationSUMO1

Identifiers

PMID35433764
PMCPMC9008726
OpenAlexW4220961406

What OpenQuestion 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 OpenQuestion graph.