Evidence map›Paper›PMID 17914349›Full record

ReviewKidney international2008

Renal response to metabolic acidosis: role of mRNA stabilization.

H Ibrahim, Y J Lee, N P Curthoys

Open access · greenAbstract readReview
In one paragraph

Review in Kidney international, 2008. 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
1.6field-weighted citation impact, top 17% 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, 59 citations in OpenAlex.

  1. Review
  2. Senolysis by GLS1 Inhibition Ameliorates Kidney Aging by Inducing Excessive mPTP Opening Through MFN1.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025
    Article
  3. Article
  4. HuR controls glutaminase RNA metabolism.Nature communications · 2024
    Article
  5. Review
  6. Investigating the Prevalence of RNA-Binding Metabolic Enzymes inInternational journal of molecular sciences · 2023
    Article
  7. Article
  8. Acid-base effects of combined renal deletion of NBCe1-A and NBCe1-B.American journal of physiology. Renal physiology · 2022
    Article
  9. Article
  10. Zeta-crystallin: a moonlighting player in cancer.Cellular and molecular life sciences : CMLS · 2020
    Review
  11. Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2020
    Article
  12. Gpr97 Exacerbates AKI by Mediating Sema3A Signaling.Journal of the American Society of Nephrology : JASN · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Expression of glutamine transporter Slc38a3 (SNAT3) during acidosis is mediated by a different mechanism than tissue-specific expression.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2014
    Article
  18. Article
  19. Review
  20. Renal ammonia metabolism and transport.Comprehensive Physiology · 2013
    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.

H IbrahimDepartment of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO 80523, USA.
Y J Lee
N P Curthoys
Colorado State University · US

Funding

CONTROL OF RENAL GLUTAMINASE INDUCTION DURING ACIDOSISR01DK037124 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CURTHOYS, NORMAN P. · 1987 to 2012
$2.7M
Regulation of Renal PEPCK Gene ExpressionR01DK043704 · NIDDK · COLORADO STATE UNIVERSITY-FORT COLLINS · PI CURTHOYS, NORMAN P. · 1991 to 2008
$1.6M
NIDDK NIH HHS DK 37124NIDDK NIH HHS DK 43704NIDDK NIH HHS R01 DK037124NIDDK NIH HHS R01 DK043704
6 · The paper itself

Abstract

The renal response to metabolic acidosis is mediated, in part, by increased expression of the genes encoding key enzymes of glutamine catabolism and various ion transporters that contribute to the increased synthesis and excretion of ammonium ions and the net production and release of bicarbonate ions. The resulting adaptations facilitate the excretion of acid and partially restore systemic acid-base balance. Much of this response may be mediated by selective stabilization of the mRNAs that encode the responsive proteins. For example, the glutaminase mRNA contains a direct repeat of 8-nt AU sequences that function as a pH-response element (pHRE). This element is both necessary and sufficient to impart a pH-responsive stabilization to chimeric mRNAs. The pHRE also binds multiple RNA-binding proteins, including zeta-crystallin (zeta-cryst), AU-factor 1 (AUF1), and HuR. The onset of acidosis initiates an endoplasmic reticulum (ER)-stress response that leads to the formation of cytoplasmic stress granules. zeta-cryst is transiently recruited to the stress granules, and concurrently, HuR is translocated from the nucleus to the cytoplasm. On the basis of the cumulative data, a mechanism for the stabilization of selective mRNAs is proposed. This hypothesis suggests multiple experiments that should define better how cells in the kidney sense very slight changes in intracellular pH and mediate this essential adaptive response.

Indexed as

Gene Expression Regulation, EnzymologicRNA StabilityAcidosisGlutaminaseGlutamineHumansHydrogen-Ion ConcentrationKidneyResponse ElementsRNA-Binding ProteinsRNA, MessengerGlutaminaseGlutamineRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID17914349
PMCPMC2814166
OpenAlexW2095084874

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.