Evidence map›Paper›PMID 29602395›Full record

ReviewSeminars in nephrology2018

The Role of Peroxisome Proliferator-Activated Receptor γ Coactivator 1α (PGC-1α) in Kidney Disease.

Szu-Yuan Li, Katalin Susztak

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Hyperlipidemia in membranous nephropathy.Clinical kidney journal · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Molecular mechanisms attributed to colistin renal proximal tubular epithelial cytotoxicity.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

13 more citing papers are in PubMed but not listed here.

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 2 countries.

Szu-Yuan LiRenal-Electrolyte and Hypertension Division, Department of Medicine, Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital and School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Katalin SusztakRenal-Electrolyte and Hypertension Division, Department of Medicine, Department of Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: ksusztak@pennmedicine.upenn.edu.
National Yang Ming Chiao Tung University · TWUniversity of Pennsylvania · US

Funding

Role of the Notch Pathway in Kidney InjuryR01DK076077 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2007 to 2026
$8.0M
Epigenetics of Chronic Kidney DiseaseR01DK087635 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI KATALIN SUSZTAK · 2009 to 2026
$7.0M
APOL1 associated kidney diseaseR01DK105821 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2016 to 2024
$4.6M
Epigenetic drivers and biomarkers of diabetic kidney diseaseDP3DK108220 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SUSZTAK, KATALIN · 2015 to 2015
$2.4M
NIDDK NIH HHS DP3 DK108220NIDDK NIH HHS R01 DK076077NIDDK NIH HHS R01 DK087635NIDDK NIH HHS R01 DK105821
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is a key transcriptional regulator of mitochondrial biogenesis and function. Several recent studies have evaluated the role of PGC-1α in various renal cell types in healthy and disease conditions. Renal tubule cells mostly depend on mitochondrial fatty acid oxidation for energy generation. A decrease in PGC-1α expression and fatty acid oxidation is commonly observed in patient samples and mouse models with acute and chronic kidney disease. Conversely, increasing PGC-1α expression in renal tubule cells restores energy deficit and has been shown to protect from acute and chronic kidney disease. Other kidney cells, such as podocytes and endothelial cells, are less metabolically active and have a narrow PGC-1α tolerance. Increasing PGC-1α levels in podocytes induces podocyte proliferation and collapsing glomerulopathy development, while increasing PGC1-α in endothelial cells alters endothelial function and causes microangiopathy, thus highlighting the cell-type-specific role of PGC-1α in different kidney cells.

Indexed as

Acute Kidney InjuryAnimalsEndothelial CellsEpithelial CellsFibrosisGene Expression RegulationGlomerulonephritisHumansKidneyKidney TubulesMitochondriaPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPodocytesRenal Insufficiency, ChronicPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanPpargc1a protein, mousemitochondriaNotchPGC-1αpodocytetubular cells

Identifiers

PMID29602395
PMCPMC5958619
OpenAlexW2794858227

What OpenQuestion holds

Textmetadata
LicenceTDM
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.