Evidence map›Paper›PMID 12374743›Full record

ArticleThe EMBO journal2002

Signaling pathways and late-onset gene induction associated with renal mesangial cell hypertrophy.

Sandro Goruppi, Joseph V Bonventre, John M Kyriakis

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. PPAR research · 2023
    Article
  3. Oncogenic Role of NUPR1 in Ovarian Cancer.OncoTargets and therapy · 2020
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Trifluoperazine Inhibits Mesangial Cell Proliferation by Arresting Cell Cycle-Dependent Mechanisms.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  9. Article
  10. Stress Response Gene Nupr1 Alleviates Cyclosporin A Nephrotoxicity In Vivo.Journal of the American Society of Nephrology : JASN · 2017
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Physiology of endothelin and the kidney.Comprehensive Physiology · 2011
    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

3 authors at 1 institution in 1 country.

Sandro GoruppiDiabetes Research Laboratory, Department of Medicine, Massachusetts General Hospital, Charlestown, MA 02129, USA.
Joseph V Bonventre
John M Kyriakis
Massachusetts General Hospital · US

Funding

MOLECULAR MEDIATORS OF DIABETIC RENAL HYPERTROPHYR01DK041513 · NIDDK · TUFTS MEDICAL CENTER · PI KYRIAKIS, JOHN M · 1990 to 2002
$631k
NIDDK NIH HHS R01-DK41513
6 · The paper itself

Abstract

In chronic diseases such as diabetes mellitus, continuous stress stimuli trigger a persistent, self-reinforcing reprogramming of cellular function and gene expression that culminates in the pathological state. Late-onset, stable changes in gene expression hold the key to understanding the molecular basis of chronic diseases. Renal failure is a common, but poorly understood complication of diabetes. Diabetic nephropathy begins with mesangial cell hypertrophy and hyperplasia, combined with excess matrix deposition. The vasoactive peptide endothelin promotes the mesangial cell hypertophy characteristic of diabetic nephropathy. In this study, we examined the signaling pathways and changes in gene expression required for endothelin-induced mesangial cell hypertrophy. Transcriptional profiling identified seven genes induced with slow kinetics by endothelin. Of these, p8, which encodes a small basic helix-loop-helix protein, was most strongly and stably induced. p8 is also induced in diabetic kidney. Mesangial cell hypertrophy and p8 induction both require activation of the ERK, JNK/SAPK and PI-3-K pathways. Small interfering RNA (siRNA)-mediated RNA interference indicates that p8 is required for endothelin-induced hypertrophy. Thus, p8 is a novel marker for diabetic renal hypertrophy.

Indexed as

Neoplasm ProteinsAnimalsBasic Helix-Loop-Helix ProteinsCells, CulturedDiabetic NephropathiesDNA-Binding ProteinsEndothelin-1Gene Expression ProfilingGene Expression RegulationGenetic MarkersGlomerular MesangiumGrowth SubstancesHumansHypertrophyJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein KinasesBasic Helix-Loop-Helix ProteinsDNA-Binding ProteinsEndothelin-1Genetic MarkersGrowth SubstancesJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein KinasesNeoplasm ProteinsNUPR1 protein, humanNupr1 protein, ratp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-Kinases

Identifiers

PMID12374743
PMCPMC129067
OpenAlexW2005431362

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.