Evidence map›Paper›PMID 27244896›Full record

ArticleOncotarget2016

Role of FOXO1 in aldosterone-induced autophagy: a compensatory protective mechanism related to podocyte injury.

Bin Wang, Wei Ding, Minmin Zhang, Hongmei Li, Honglei Guo, Lilu Lin, Jing Chen, Yong Gu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. SIRT1 Promotes Host Protective Immunity againstInternational journal of molecular sciences · 2022
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. FOXO1 overexpression is correlated with poor prognosis in epithelial ovarian cancer.Cancer biomarkers : section A of Disease markers · 2020
    Article
  14. Article
  15. Connexin 43‑autophagy loop in the podocyte injury of diabetic nephropathy.International journal of molecular medicine · 2019
    Article
  16. Article
  17. Article
  18. 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

8 authors at 3 institutions in 1 country.

Bin WangDivision of Nephrology, Huashan Hospital and Institute of Nephrology, Fudan University, Shanghai, China.
Wei DingDivision of Nephrology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
Minmin ZhangDivision of Nephrology, Huashan Hospital and Institute of Nephrology, Fudan University, Shanghai, China.
Hongmei LiDivision of Nephrology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Honglei GuoDivision of Nephrology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Lilu LinDivision of Nephrology, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai, China.
Jing ChenDivision of Nephrology, Huashan Hospital and Institute of Nephrology, Fudan University, Shanghai, China.
Yong GuDivision of Nephrology, Huashan Hospital and Institute of Nephrology, Fudan University, Shanghai, China.
Fudan University · CNHuashan Hospital · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was undertaken to elucidate whether and how autophagy was regulated in aldosterone (Aldo)-induced podocyte injury and to examine its role in this model both in vitro and in vivo. In cultured podocytes, Aldo increased autophagy flux as indicated by the enhanced expression of LC3-II/LC3-I and the reduction of p62. Autophagy induction with rapamycin (RP) provided a cytoprotective effect, and inhibition of autophagy with Atg7-specific siRNA, chloroquine (CQ) or 3-methyladenine (3-MA) worsened Aldo-induced podocyte injury by attenuating endoplasmic reticulum (ER) stress. Aldo inhibited Akt phosphorylation but increased the mammalian target of rapamycin (mTOR) signaling pathway; however, Aldo up-regulated the expression of FOXO1 and its downstream effector Rab7. Either knockdown of FOXO1 or Rab7 inhibited Aldo-induced autophagy. Additionally, an elevated level of P300-regulated acetylation of FOXO1 and the interaction of acetylated FOXO1 and Atg7 were also confirmed to be involved in regulating autophagy in Aldo-induced podocytes. Similar results were further confirmed in vivo. We propose that autophagy enhancement through enhancing of the FOXO1/Rab7 axis and post-translational modification of FOXO1 may represent a potential therapeutic strategy against podocyte injury by promoting autophagy.

Indexed as

AldosteroneAnimalsAutophagyCells, CulturedEndoplasmic Reticulum StressForkhead Box Protein O1MaleMiceNerve Tissue ProteinsPodocytesProto-Oncogene Proteins c-aktrab7 GTP-Binding Proteinsrab GTP-Binding ProteinsRatsRats, Sprague-DawleySignal TransductionAldosteroneForkhead Box Protein O1Foxo1 protein, ratmTOR protein, ratNerve Tissue ProteinsProto-Oncogene Proteins c-aktrab7 GTP-Binding Proteinsrab7 GTP-binding proteins, mouserab7 GTP-binding proteins, ratrab GTP-Binding ProteinsTOR Serine-Threonine KinasesaldosteroneapoptosisautophagyFOXO1podocyte

Identifiers

PMID27244896
PMCPMC5216726
OpenAlexW2405753991

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.