Evidence map›Paper›PMID 33934104›Full record

ArticleCell death and differentiation2021

PP2Acα promotes macrophage accumulation and activation to exacerbate tubular cell death and kidney fibrosis through activating Rap1 and TNFα production.

Yan Liang, Xiaoli Sun, Mingjie Wang, Qingmiao Lu, Mengru Gu, Lu Zhou, Qing Hou, Mengzhu Tan, Sudan Wang, Xian Xue and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  10. Review
  11. Relaxin in fibrotic ligament diseases: Its regulatory role and mechanism.Frontiers in cell and developmental biology · 2023
    Review
  12. Article
  13. MicroRNA-382 Promotes M2-Like MacrophageFrontiers in immunology · 2022
    Article
  14. 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

11 authors at 2 institutions in 1 country.

Yan LiangCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Xiaoli SunDepartment of Clinical Genetics, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Mingjie WangCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Qingmiao LuCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Mengru GuCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Lu ZhouCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Qing HouCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Mengzhu TanCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Sudan WangCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Xian XueDepartment of Clinical Genetics, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Chunsun DaiCenter for Kidney Disease, the 2nd Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu, China. daichunsun@njmu.edu.cn.ORCID http://orcid.org/0000-0001-7616-2469
Nanjing Medical University · CNNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage accumulation and activation play an essential role in kidney fibrosis; however, the underlying mechanisms remain to be explored. By analyzing the kidney tissues from patients and animal models with kidney fibrosis, we found a large induction of PP2Acα in macrophages. We then generated a mouse model with inducible macrophage ablation of PP2Acα. The knockouts developed less renal fibrosis, macrophage accumulation, or tubular cell death after unilateral ureter obstruction or ischemic reperfusion injury compared to control littermates. In cultured macrophages, PP2Acα deficiency resulted in decreased cell motility by inhibiting Rap1 activity. Moreover, co-culture of PP2Acα

Indexed as

AnimalsCells, CulturedDisease Models, AnimalFibrosisHumansMacrophagesMaleMiceProtein Phosphatase 2Crap1 GTP-Binding ProteinsRenal Insufficiency, ChronicSignal TransductionTransfectionTumor Necrosis Factor-alphaPpm1a protein, mouseProtein Phosphatase 2Crap1 GTP-Binding ProteinsRap1 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID33934104
PMCPMC8408198
OpenAlexW3158203860

What OpenQuestion 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 OpenQuestion graph.