Evidence map›Paper›PMID 30120380›Full record

ReviewNature reviews. Nephrology2018

Metabolism and mitochondria in polycystic kidney disease research and therapy.

Valeria Padovano, Christine Podrini, Alessandra Boletta, Michael J Caplan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 1 pooled it
14.8field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Review
  8. Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026
    Article
  9. Article
  10. Article
  11. The Role of Mitochondria in Polycystic Kidney Disease.International journal of molecular sciences · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

47 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

4 authors at 1 institution in 1 country.

Valeria PadovanoDepartment of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, CT, USA.
Christine PodriniDivision of Genetics and Cell Biology, Dibit, San Raffaele Scientific Institute, Milan, Italy.ORCID http://orcid.org/0000-0002-5391-3378
Alessandra BolettaDivision of Genetics and Cell Biology, Dibit, San Raffaele Scientific Institute, Milan, Italy.
Michael J CaplanDepartment of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, CT, USA. michael.caplan@yale.edu.
Yale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common, potentially lethal, monogenic diseases and is caused predominantly by mutations in polycystic kidney disease 1 (PKD1) and PKD2, which encode polycystin 1 (PC1) and PC2, respectively. Over the decades-long course of the disease, patients develop large fluid-filled renal cysts that impair kidney function, leading to end-stage renal disease in ~50% of patients. Despite the identification of numerous dysregulated pathways in ADPKD, the molecular mechanisms underlying the renal dysfunction from mutations in PKD genes and the physiological functions of the polycystin proteins are still unclear. Alterations in cell metabolism have emerged in the past decade as a hallmark of ADPKD. ADPKD cells shift their mode of energy production from oxidative phosphorylation to alternative pathways, such as glycolysis. In addition, the polycystins seem to play regulatory roles in modulating mechanisms and machinery related to energy production and utilization, including AMPK, PPARα, PGC1α, calcium signalling at mitochondria-associated membranes, mTORC1, cAMP and CFTR-mediated ion transport as well as the expression of crucial components of the mitochondrial energy production apparatus. In this Review, we explore these metabolic changes and discuss in detail the relationship between energy metabolism and ADPKD pathogenesis and identify potential therapeutic targets.

Indexed as

Energy MetabolismMolecular Targeted TherapyAMP-Activated Protein KinasesAnimalsCyclic AMPFatty AcidsGlucoseGlycolysisHumansLipid MetabolismMechanistic Target of Rapamycin Complex 1MitochondriaOxidation-ReductionPolycystic Kidney, Autosomal DominantSignal TransductionAMP-Activated Protein KinasesCyclic AMPFatty AcidsGlucoseMechanistic Target of Rapamycin Complex 1

Identifiers

PMID30120380
OpenAlexW2887872978

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.