Evidence map›Paper›PMID 33013450›Full record

ReviewFrontiers in physiology2020

Dyslipidemia in Kidney Disorders: Perspectives on Mitochondria Homeostasis and Therapeutic Opportunities.

Pei-Hui Lin, Pu Duann

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Review
  6. Chronic exposure to low levels of glyphosate and metals induces kidney dysfunction.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  7. Chronic NHScientific reports · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
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  15. Review
  16. Review
  17. Article
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  19. Article
  20. Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023
    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

2 authors at 2 institutions in 1 country.

Pei-Hui LinDepartment of Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, United States.
Pu DuannResearch and Development, Salem Veteran Affairs Medical Center, Salem, VA, United States.
Salem VA Medical Center · USThe Ohio State University · US

Funding

Targeting cell membrane repair for treatment of acute kidney injuryR01DK106394 · NIDDK · OHIO STATE UNIVERSITY · PI LIN, PEI-HUI, ROVIN, BRAD H · 2016 to 2020
$2.5M
NIDDK NIH HHS R01 DK106394
6 · The paper itself

Abstract

To excrete body nitrogen waste and regulate electrolyte and fluid balance, the kidney has developed into an energy factory with only second to the heart in mitochondrial content in the body to meet the high-energy demand and regulate homeostasis. Energy supply from the renal mitochondria majorly depends on lipid metabolism, with programed enzyme systems in fatty acid β-oxidation and Krebs cycle. Renal mitochondria integrate several metabolic pathways, including AMPK/PGC-1α, PPARs, and CD36 signaling to maintain energy homeostasis for dynamic and static requirements. The pathobiology of several kidney disorders, including diabetic nephropathy, acute and chronic kidney injuries, has been primarily linked to impaired mitochondrial bioenergetics. Such homeostatic disruption in turn stimulates a pathological adaptation, with mitochondrial enzyme system reprograming possibly leading to dyslipidemia. However, this alteration, while rescuing oncotic pressure deficit secondary to albuminuria and dissipating edematous disorder, also imposes an ominous lipotoxic consequence. Reprograming of lipid metabolism in kidney injury is essential to preserve the integrity of kidney mitochondria, thereby preventing massive collateral damage including excessive autophagy and chronic inflammation. Here, we review dyslipidemia in kidney disorders and the most recent advances on targeting mitochondrial energy metabolism as a therapeutic strategy to restrict renal lipotoxicity, achieve salutary anti-edematous effects, and restore mitochondrial homeostasis.

Indexed as

energy metabolismfatty acid β-oxidationfibrosishomeostasislipotoxicityoxidative stresspodocyteproximal tubule cells

Identifiers

PMID33013450
PMCPMC7494972
OpenAlexW3083356227

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.