Evidence map›Paper›PMID 33861526›Full record

ReviewCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2021

Podocyte Sphingolipid Signaling in Nephrotic Syndrome.

Guangbi Li, Jason Kidd, Todd W B Gehr, Pin-Lan Li

Open access · goldAbstract readReview
In one paragraph

Review in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2021. 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
1.6field-weighted citation impact, top 17% 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, 18 citations in OpenAlex.

  1. Review
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  7. Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025
    Review
  8. Article
  9. Article
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  12. Article
  13. Review
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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.

Guangbi LiDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Jason KiddDivision of Nephrology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Todd W B GehrDivision of Nephrology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA.
Pin-Lan LiDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, USA, pin-lan.li@vcuhealth.org.
Virginia Commonwealth University · US

Funding

Hypertension and glomerular injury in hyperhomocysteinemia - role of inflammatory exosomesR01DK054927 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 1998 to 2023
$6.7M
Lysosome dysfunction in podocytopathy and associated hypertensionR01DK120491 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2018 to 2022
$2.4M
NIDDK NIH HHS R01 DK054927NIDDK NIH HHS R01 DK120491NIH (National Institutes of Health) DK054927, DK120491
6 · The paper itself

Abstract

Podocytes play a vital role in the pathogenesis of nephrotic syndrome (NS), which is clinically characterized by heavy proteinuria, hypoalbuminemia, hyperlipidemia, and peripheral edema. The pathogenesis of NS has evolved through several hypotheses ranging from immune dysregulation theory and increased glomerular permeability theory to the current concept of podocytopathy. Podocytopathy is characterized by dysfunction or depletion of podocytes, which may be caused by unknown permeability factor, genetic disorders, drugs, infections, systemic disorders, and hyperfiltration. Over the last two decades, numerous studies have been done to explore the molecular mechanisms of podocyte injuries or NS and to develop the novel therapeutic strategies targeting podocytopathy for treatment of NS. Recent studies have shown that normal sphingolipid metabolism is essential for structural and functional integrity of podocytes. As a basic component of the plasma membrane, sphingolipids not only support the assembly of signaling molecules and interaction of receptors and effectors, but also mediate various cellular activities, such as apoptosis, proliferation, stress responses, necrosis, inflammation, autophagy, senescence, and differentiation. This review briefly summarizes current evidence demonstrating the regulation of sphingolipid metabolism in podocytes and the canonical or noncanonical roles of podocyte sphingolipid signaling in the pathogenesis of NS and associated therapeutic strategies.

Indexed as

Signal TransductionAnimalsHumansMetabolic Networks and PathwaysNephrotic SyndromePodocytesSphingolipidsSphingolipidsSphingolipid; Acid ceramidase; Sphingomyelin-like phosphodiesterase 3b; Podocyte; Nephrotic syndrome

Identifiers

PMID33861526
PMCPMC8193717
OpenAlexW3154919486

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.