Evidence map›Paper›PMID 27097894›Full record

ReviewAmerican journal of physiology. Renal physiology2016

The podocyte as a direct target for treatment of glomerular disease?

Sandeep K Mallipattu, John C He

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

48 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Blood Pressure Management Strategies and Podocyte Health.American journal of hypertension · 2025
    Review
  6. Article
  7. A Small Molecule Agonist of Krüppel-Like Factor 15 in Proteinuric Kidney Disease.Journal of the American Society of Nephrology : JASN · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Modeling ofKidney international reports · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

2 authors at 2 institutions in 1 country.

Sandeep K MallipattuDivision of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York;
John C HeDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; and Renal Section, James J. Peters VA Medical Center, New York, New York cijiang.he@mssm.edu.
James J. Peters VA Medical Center · USStony Brook University · US

Funding

Cellular and molecular mechanisms of retinoids in podocytesR01DK078897 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI HE, JOHN CIJIANG · 2007 to 2018
$3.6M
The Role of KLF15 as a transcriptional regulator of podocyte differentiationK08DK102519 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI MALLIPATTU, SANDEEP K · 2014 to 2018
$917k
NIDDK NIH HHS K08 DK102519NIDDK NIH HHS R01 DK078897
6 · The paper itself

Abstract

The Centers for Disease Control and Prevention estimates more than 10% of adults in the United States, over 20 million Americans, have chronic kidney disease (CKD). A failure to maintain the glomerular filtration barrier directly contributes to the onset of CKD. The visceral epithelial cells, podocytes, are integral to the maintenance of this renal filtration barrier. Direct podocyte injury contributes to the onset and progression of glomerular diseases such as minimal change disease (MCD), focal segmental glomerular sclerosis (FSGS), diabetic nephropathy, and HIV-associated nephropathy (HIVAN). Since podocytes are terminally differentiated with minimal capacity to self-replicate, they are extremely sensitive to cellular injury. In the past two decades, our understanding of the mechanism(s) by which podocyte injury occurs has greatly expanded. With this newfound knowledge, therapeutic strategies have shifted to identifying targets directed specifically at the podocyte. Although the systemic effects of these agents are important, their direct effect on the podocyte proves to be essential in ameliorating glomerular disease. In this review, we highlight the mechanisms by which these agents directly target the podocyte independent of its systemic effects.

Indexed as

AnimalsCalcineurin InhibitorsGlucocorticoidsHumansKidney GlomerulusPodocytesRenal Insufficiency, ChronicCalcineurin InhibitorsGlucocorticoidsabataceptcalcineurin inhibitorsglucocorticoidspodocyterituximab

Identifiers

PMID27097894
PMCPMC4967158
OpenAlexW2340540849

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.