Evidence map›Paper›PMID 26180237›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Simultaneous deletion of Bax and Bak is required to prevent apoptosis and interstitial fibrosis in obstructive nephropathy.

Hee-Seong Jang, Babu J Padanilam

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Article
  7. p53 and Myofibroblast Apoptosis in Organ Fibrosis.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Cell Death in the Kidney.International journal of molecular sciences · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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.

Hee-Seong JangDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and.
Babu J PadanilamDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and Department of Internal Medicine, Section of Nephrology, University of Nebraska Medical Center, Omaha, Nebraska bpadanilam@unmc.edu.
University of Nebraska Medical Center · US

Funding

Regulation of Apoptosis in Renal IschemiaR01DK083291 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PADANILAM, BABU JOSEPH · 2010 to 2013
$1.3M
NIDDK NIH HHS DK-083291NIDDK NIH HHS R01 DK083291
6 · The paper itself

Abstract

Proximal tubular injury and apoptosis are key mediators of the development of kidney fibrosis, a hallmark of chronic kidney disease. However, the molecular mechanism by which tubular apoptotic cell death leads to kidney fibrosis is poorly understood. In the present study, we tested the roles of Bcl-2-associated X (Bax) and Bcl-2 antagonist/killer (Bak), two crucial proteins involved in intrinsic apoptotic cell death, in the progression of kidney fibrosis. Mice with proximal tubule-specific Bax deletion, systemic deletion of Bak, and dual deletion of Bax and Bak were subjected to unilateral ureteral obstruction (UUO). Dual deficiency of Bax and Bak inhibited tubular apoptosis and atrophy. Consistent with decreased tubular injury, dual ablation of Bax and Bak suppressed UUO-induced inflammation and kidney fibrosis with decreased tubular cell cycle arrest, expression of fibrogenic and inflammatory cytokines, and oxidative stress in the kidney. Bax or Bak deficiency was insufficient to prevent apoptosis and all other aforementioned malevolent effects, suggesting compensatory mediation by each other in the respective signaling pathways. These data suggest that dual ablation of Bax and Bak in the kidney is required to prevent UUO-induced tubular apoptosis and the consequent kidney inflammation and fibrosis.

Indexed as

AnimalsApoptosisbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinCollagenFibrosisGene DeletionKidneyKidney DiseasesKidney TubulesLipid PeroxidationMiceMice, Inbred C57BLMice, KnockoutUreteral Obstructionbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinCollagenapoptosisBcl-2 antagonist/killerBcl-2-associated Xchronic kidney diseasefibrosisinflammationoxidative stress

Identifiers

PMID26180237
PMCPMC4572396
OpenAlexW2220751146

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.