Evidence map›Paper›PMID 36263179›Full record

ArticleInternational journal of biological sciences2022

Anp32e promotes renal interstitial fibrosis by upregulating the expression of fibrosis-related proteins.

Ju Wei, Yi Shan, Zheng Xiao, Lu Wen, Yilin Tao, Xi Fang, Hanwen Luo, Chengyuan Tang, Ying Li

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

9 authors at 1 institution in 1 country.

Ju WeiDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Yi ShanDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Zheng XiaoDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Lu WenDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Yilin TaoDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Xi FangDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Hanwen LuoDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Chengyuan TangDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Ying LiDepartment of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, 410011, Hunan, China.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acidic nuclear phosphoprotein 32 family member e (Anp32e) has been reported to contribute to early mammalian development and cancer metastasis. However, the pathophysiological role of Anp32e in renal interstitial fibrosis (RIF) is poorly understood. Here, we demonstrated that Anp32e was highly expressed in the region of RIF in patients with IgA nephropathy, unilateral ureteral obstruction (UUO) mouse kidneys, and Boston University mouse proximal tubular (BUMPT) cells when treated with TGF-β1; this upregulation was positively correlated with the total fibrotic area of the kidneys. The overexpression of Anp32e enhanced the TGF-β1-induced production of fibrosis-related proteins (fibronectin (Fn) and collagen type I (Col-I)) in BUMPT cells whereas the knockdown of Anp32e suppressed the deposition of these fibrosis-related proteins in UUO mice and TGF-β1-stimulated BUMPT cells. In particular, Anp32e overexpression alone induced the deposition of Fn and Col-I in both mouse kidneys and BUMPT cells without TGF-β1 stimulation. Furthermore, we revealed that the overexpression of Anp32e induced the expression of TGF-β1 and p-Smad3 while TGF-β1 inhibitor SB431542 reversed the Anp32e-induced upregulation of Fn and Col-I in BUMPT cells without TGF-β1 stimulation. Collectively, our data demonstrate that Anp32e promotes the deposition of fibrosis-related proteins by regulating the TGF-β1/Smad3 pathway.

Indexed as

Kidney DiseasesMolecular ChaperonesAnimalsCell LineCollagen Type IFibronectinsFibrosisKidneyMammalsMiceSignal TransductionTransforming Growth Factor beta1Ureteral ObstructionAnp32e protein, mouseCollagen Type IFibronectinsMolecular ChaperonesTransforming Growth Factor beta1Anp32eCKDfibrosis-related proteinpro-fibrotic factorrenal interstitial fibrosisTGF-β1/Smad3

Identifiers

PMID36263179
PMCPMC9576520
OpenAlexW4306912939

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.