Evidence map›Paper›PMID 24817115›Full record

ArticleThe Journal of biological chemistry2014

Reduction of proteinuria through podocyte alkalinization.

Mehmet M Altintas, Kumiko Moriwaki, Changli Wei, Clemens C Möller, Jan Flesche, Jing Li, Suma Yaddanapudi, Mohd Hafeez Faridi, Markus Gödel, Tobias B Huber and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Glutaminolysis is a Potential Therapeutic Target for Kidney Diseases.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  9. Article
  10. Article
  11. Mechanisms of Metabolic Acidosis-Induced Kidney Injury in Chronic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2020
    Article
  12. Article
  13. N-Degradomic Analysis Reveals a Proteolytic Network Processing the Podocyte Cytoskeleton.Journal of the American Society of Nephrology : JASN · 2017
    Article
  14. Review
  15. Podocytes.F1000Research · 2016
    Review
  16. 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

15 authors at 7 institutions in 3 countries.

Mehmet M AltintasFrom the Department of Medicine, Rush University Medical Center, Chicago, Illinois 60035.
Kumiko Moriwakithe Department of Medicine, Division of Nephrology and Hypertension, University of Miami Miller School of Medicine, Miami, Florida 33136.
Changli WeiFrom the Department of Medicine, Rush University Medical Center, Chicago, Illinois 60035.
Clemens C Möllerthe Division of Nephrology and Program in Glomerular Disease, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129.
Jan Fleschethe Division of Nephrology and Program in Glomerular Disease, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129.
Jing LiFrom the Department of Medicine, Rush University Medical Center, Chicago, Illinois 60035.
Suma Yaddanapudithe Division of Nephrology and Program in Glomerular Disease, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129.
Mohd Hafeez FaridiFrom the Department of Medicine, Rush University Medical Center, Chicago, Illinois 60035.
Markus Gödelthe Renal Division, University Hospital Freiburg, 79106 Freiburg, Germany.
Tobias B Huberthe Renal Division, University Hospital Freiburg, 79106 Freiburg, Germany, the BIOSS Centre for Biological Signalling Studies, Albert-Ludwigs University, 79106 Freiburg, Germany.
Richard A Prestonthe Department of Medicine, Division of Clinical Pharmacology, University of Miami Miller School of Medicine, Miami, Florida 33136.
Jean X Jiangthe Department of Biochemistry, University of Texas Health Science Center, San Antonio, Texas 78229, and.
Dontscho Kerjaschkithe Clinical Institute of Pathology, Medical University of Vienna, 1090 Vienna, Austria.
Sanja Severthe Division of Nephrology and Program in Glomerular Disease, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129.
Jochen ReiserFrom the Department of Medicine, Rush University Medical Center, Chicago, Illinois 60035, jochen_reiser@rush.edu.
Rush University Medical Center · USMassachusetts General Hospital · USUniversity Medical Center Freiburg · DEUniversity of Miami · USHarvard University · USMedical University of Vienna · ATThe University of Texas Health Science Center at San Antonio · US

Funding

Proteolytic Regulation of Podocyte Function by Cathepsin L.R01DK073495 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI REISER, JOCHEN · 2006 to 2015
$2.4M
NIDDK NIH HHS DK073495NIDDK NIH HHS R01 DK073495
6 · The paper itself

Abstract

Podocytes are highly differentiated cells and critical elements for the filtration barrier of the kidney. Loss of their foot process (FP) architecture (FP effacement) results in urinary protein loss. Here we show a novel role for the neutral amino acid glutamine in structural and functional regulation of the kidney filtration barrier. Metabolic flux analysis of cultured podocytes using genetic, toxic, and immunologic injury models identified increased glutamine utilization pathways. We show that glutamine uptake is increased in diseased podocytes to couple nutrient support to increased demand during the disease state of FP effacement. This feature can be utilized to transport increased amounts of glutamine into damaged podocytes. The availability of glutamine determines the regulation of podocyte intracellular pH (pHi). Podocyte alkalinization reduces cytosolic cathepsin L protease activity and protects the podocyte cytoskeleton. Podocyte glutamine supplementation reduces proteinuria in LPS-treated mice, whereas acidification increases glomerular injury. In summary, our data provide a metabolic opportunity to combat urinary protein loss through modulation of podocyte amino acid utilization and pHi.

Indexed as

AnimalsBiological Transport, ActiveCells, CulturedCytoskeletonHydrogen-Ion ConcentrationMiceMice, KnockoutPodocytesProteinuriaCell pHGlutamineLipopolysaccharide (LPS)MetabolismPodocyte

Identifiers

PMID24817115
PMCPMC4067184
OpenAlexW1978188233

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.