Evidence map›Paper›PMID 20581056›Full record

ArticleThe American journal of pathology2010

HIV-associated nephropathy: role of mammalian target of rapamycin pathway.

Dileep Kumar, Sridevi Konkimalla, Anju Yadav, Kavithalakshmi Sataranatarajan, Balakuntalam S Kasinath, Praveen N Chander, Pravin C Singhal

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. 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
3.1field-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

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Vascular Growth Factors and Glomerular Disease.Annual review of physiology · 2016
    Review
  12. Article
  13. Article
  14. mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN.American journal of physiology. Renal physiology · 2013
    Article
  15. Article
  16. MicroRNAs in HIV-associated nephropathy (HIVAN).Experimental and molecular pathology · 2013
    Article
  17. Article
  18. Article
  19. Constitutive activation of the mTOR signaling pathway within the normal glomerulus.Biochemical and biophysical research communications · 2012
    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

7 authors at 3 institutions in 1 country.

Dileep KumarDepartment of Immunology, Feinstein Institute for Medical Research, Manhasset, New York, USA.
Sridevi Konkimalla
Anju Yadav
Kavithalakshmi Sataranatarajan
Balakuntalam S Kasinath
Praveen N Chander
Pravin C Singhal
Feinstein Institute for Medical Research · USThe University of Texas Health Science Center at San Antonio · USNew York Medical College · US

Funding

p66ShcA in HIV associated NephropathyR01DK083931 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2010 to 2013
$2.5M
Renin Angioensin Aldosterone System in Drub Abuse and HIV-associated NephropathyR01DK084910 · NIDDK · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SINGHAL, PRAVIN C · 2010 to 2014
$1.7M
Novel mechanisms of diabetic nephropathyR01DK077295 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KASINATH, BALAKUNTALAM S · 2007 to 2011
$1.3M
NIDDK NIH HHS R01 DK077295NIDDK NIH HHS R01 DK083931NIDDK NIH HHS R01 DK084910
6 · The paper itself

Abstract

Both glomerular and tubular lesions are characterized by a proliferative phenotype in HIV-associated nephropathy. We hypothesized that mammalian target of rapamycin (mTOR) contributes to the development of the HIVAN phenotype. Both glomerular and tubular epithelial cells showed enhanced expression of phospho (p)-mTOR in HIV-1 transgenic mice (Tgs). In addition, renal tissues of transgenic mice (RT-Tg) showed enhanced phosphorylation of p70S6 kinase and an associated diminished phosphorylation of eEF2. Moreover, RT-Tgs showed enhanced phosphorylation of 4EBP1 and eIF4B; these findings indicated activation of the mTOR pathway in RT-Tgs. To test our hypothesis, age- and sex-matched control mice and Tgs were administered either saline or rapamycin (an inhibitor of the mTOR pathway) for 4 weeks. Tgs receiving rapamycin not only showed inhibition of the mTOR-associated downstream signaling but also displayed attenuated renal lesions. RT-Tgs showed enhanced expression of hypoxia-inducible factor-alpha and also displayed increased expression of vascular endothelial growth factor; on the other hand, rapamycin inhibited RT-Tg expression of both hypoxia-inducible factor-alpha and vascular endothelial growth factor. We conclude that the mTOR pathway contributes to the HIVAN phenotype and that inhibition of the mTOR pathway can be used as a therapeutic strategy to alter the course of HIVAN.

Indexed as

AIDS-Associated NephropathyAnimalsHumansHypoxia-Inducible Factor 1, alpha SubunitKidney GlomerulusKidney TubulesMaleMiceMice, TransgenicPhenotypeRibosomal Protein S6 Kinases, 70-kDaSignal TransductionTOR Serine-Threonine KinasesVascular Endothelial Growth Factor AHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitRibosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine KinasesVascular Endothelial Growth Factor A

Identifiers

PMID20581056
PMCPMC2913356
OpenAlexW1627653490

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.