Evidence map›Paper›PMID 26990086›Full record

ArticlePloS one2016

Autophagy Limits Endotoxemic Acute Kidney Injury and Alters Renal Tubular Epithelial Cell Cytokine Expression.

Jeremy S Leventhal, Jie Ni, Morgan Osmond, Kyung Lee, G Luca Gusella, Fadi Salem, Michael J Ross

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  12. Protective effect of HMolecular medicine reports · 2022
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Autophagy in kidney homeostasis and disease.Nature reviews. Nephrology · 2020
    Review
  20. Myoglobin Mediates Autophagy of NRK-52E in Rat Renal Tubular Epithelial Cells Via the Pink1/Parkin Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020
    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

7 authors at 1 institution in 1 country.

Jeremy S LeventhalDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Jie NiDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Morgan OsmondDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Kyung LeeDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
G Luca GusellaDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Fadi SalemDepartment of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Michael J RossDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Icahn School of Medicine at Mount Sinai · US

Funding

Novel mechanisms of antiretroviral protection against HIV-related kidney diseasesR01DK101338 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ROSS, MICHAEL J · 2014 to 2018
$1.9M
The role of APOL1 polymorphisms in promoting HIV-related kidney injuryR01DK108346 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ROSS, MICHAEL J · 2015 to 2019
$1.6M
The Role of Autophagy in LPS-Induced Acute Kidney InjuryK08DK090217 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEVENTHAL, JEREMY SETH · 2013 to 2017
$755k
NIDDK NIH HHS DK108346NIDDK NIH HHS K08 DK090217NIDDK NIH HHS R01 DK101338NIDDK NIH HHS R01 DK108346PHS HHS NIDDK K08 DK090217
6 · The paper itself

Abstract

Sepsis related acute kidney injury (AKI) is a common in-hospital complication with a dismal prognosis. Our incomplete understanding of disease pathogenesis has prevented the identification of hypothesis-driven preventive or therapeutic interventions. Increasing evidence in ischemia-reperfusion and nephrotoxic mouse models of AKI support the theory that autophagy protects renal tubular epithelial cells (RTEC) from injury. However, the role of RTEC autophagy in septic AKI remains unclear. We observed that lipopolysaccharide (LPS), a mediator of gram-negative bacterial sepsis, induces RTEC autophagy in vivo and in vitro through TLR4-initiated signaling. We modeled septic AKI through intraperitoneal LPS injection in mice in which autophagy-related protein 7 was specifically knocked out in the renal proximal tubules (ATG7KO). Compared to control littermates, ATG7KO mice developed more severe renal dysfunction (24hr BUN 100.1mg/dl +/- 14.8 vs 54.6mg/dl +/- 11.3) and parenchymal injury. After injection with LPS, analysis of kidney lysates identified higher IL-6 expression and increased STAT3 activation in kidney lysates from ATG7KO mice compared to controls. In vitro experiments confirmed an altered response to LPS in RTEC with genetic or pharmacological impairment of autophagy. In conclusion, RTEC autophagy protects against endotoxin induced injury and regulates downstream effects of RTEC TLR4 signaling.

Indexed as

AutophagyAcute Kidney InjuryAnimalsCell LineCytokinesEndotoxemiaEpithelial CellsKidney TubulesMiceMice, Inbred C57BLCytokines

Identifiers

PMID26990086
PMCPMC4798771
OpenAlexW2297711016

What OpenQuestion holds

Textmetadata
LicenceCC0
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.