Evidence map›Paper›PMID 26081285›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2015

(Pro)renin receptor regulates autophagy and apoptosis in podocytes exposed to high glucose.

Caixia Li, Helmy M Siragy

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. The (pro)renin receptor in health and disease.Nature reviews. Nephrology · 2019
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Caixia LiDivision of Endocrinology and Metabolism, University of Virginia Health System, Charlottesville, Virginia.
Helmy M SiragyDivision of Endocrinology and Metabolism, University of Virginia Health System, Charlottesville, Virginia hms7a@virginia.edu.
University of Virginia Health System · US

Funding

Prorenin Receptors Mediate Hypertension and Kidney Disease in DiabetesR01HL091535 · NHLBI · UNIVERSITY OF VIRGINIA · PI SIRAGY, HELMY M · 2008 to 2020
$5.1M
Renin receptor provoked renal inflammationR01DK078757 · NIDDK · UNIVERSITY OF VIRGINIA · PI SIRAGY, HELMY M · 2007 to 2016
$3.3M
NHLBI NIH HHS HL-091535NIDDK NIH HHS DK-078757
6 · The paper itself

Abstract

High glucose reduces autophagy and enhances apoptosis of podocytes. Previously, we reported that high glucose induced podocyte injury through upregulation of the (pro)renin receptor (PRR). We hypothesized that increasing PRR reduces autophagy and increases apoptosis of mouse podocytes exposed to high glucose via activation of the PI3K/Akt/mTOR signaling pathway. Mouse podocytes were cultured in normal (5 mmol/l) or high (25 mmol/l) d-glucose for 48 h. High glucose significantly increased mRNA and protein levels of PRR, phosphorylation of PI3K/Akt/mTOR, and p62. In contrast, high glucose decreased activation of UNC-51-like kinase-1 (ULK1) by phosphorylating Ser⁷⁵⁷ and protein levels of microtubule-associated protein-1 light chain 3B (LC3B)-II and Lamp-2. Bafilomycin A1 increased LC3BII and p62 accumulation in high-glucose-treated cells. High glucose reduced the autophagic flux. Confocal microscopy studies showed significant reduction in the protein level of LC3B in response to high glucose. Cyto-ID autophagy staining showed a significant decrease in autophagosome formation with high glucose. In the absence of PRR, activation of Akt with sc-79 or mTOR with MHY-1485 increased p62 accumulation. Caspase-3/7 activity and apoptosis monitored by TUNEL assay were significantly increased in podocytes treated with high glucose. PRR siRNA significantly reversed the effects of high glucose. Based on these data, we conclude that high glucose decreases autophagy and increases apoptosis in mouse podocytes through the PRR/PI3K/Akt/mTOR signaling pathway.

Indexed as

ApoptosisAutophagySignal TransductionAnimalsAutophagy-Related Protein-1 HomologCell LineGlucoseHyperglycemiaLysosomal-Associated Membrane Protein 2MiceMicrotubule-Associated ProteinsOsmolar ConcentrationPhosphatidylinositol 3-KinasePhosphorylationPodocytesProrenin ReceptorATP6AP2 protein, mouseAutophagy-Related Protein-1 HomologGlucoseLysosomal-Associated Membrane Protein 2Map1lc3b protein, mouseMicrotubule-Associated ProteinsmTOR protein, mouseMyc protein, mousePhosphatidylinositol 3-KinaseProrenin ReceptorProtein Serine-Threonine KinasesProton-Translocating ATPasesProto-Oncogene Proteins c-mycReceptors, Cell SurfaceTOR Serine-Threonine KinasesUlk1 protein, mouseapoptosisautophagyhigh glucosepodocyte(pro)renin receptor

Identifiers

PMID26081285
PMCPMC4525115
OpenAlexW2177131501

What OpenQuestion holds

Textmetadata
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.