Evidence map›Paper›PMID 35457062›Full record

ReviewInternational journal of molecular sciences2022

Implications of Sphingolipid Metabolites in Kidney Diseases.

Shamroop Kumar Mallela, Sandra Merscher, Alessia Fornoni

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 35 citations in OpenAlex.

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  15. Article
  16. Sphingolipids and Chronic Kidney Disease.Journal of clinical medicine · 2024
    Review
  17. Article
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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

3 authors at 1 institution in 1 country.

Shamroop Kumar MallelaKatz Family Division of Nephrology and Hypertension, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Sandra MerscherKatz Family Division of Nephrology and Hypertension, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Alessia FornoniKatz Family Division of Nephrology and Hypertension, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
University of Miami · US

Funding

Miami Clinical Translational Science Institute U54DK083912, UM1DK100846, U01DK116101 and UL1TR000460NIH HHS R01DK117599, R01DK104753, R01CA227493
6 · The paper itself

Abstract

Sphingolipids, which act as a bioactive signaling molecules, are involved in several cellular processes such as cell survival, proliferation, migration and apoptosis. An imbalance in the levels of sphingolipids can be lethal to cells. Abnormalities in the levels of sphingolipids are associated with several human diseases including kidney diseases. Several studies demonstrate that sphingolipids play an important role in maintaining proper renal function. Sphingolipids can alter the glomerular filtration barrier by affecting the functioning of podocytes, which are key cellular components of the glomerular filtration barrier. This review summarizes the studies in our understanding of the regulation of sphingolipid signaling in kidney diseases, especially in glomerular and tubulointerstitial diseases, and the potential to target sphingolipid pathways in developing therapeutics for the treatment of renal diseases.

Indexed as

Kidney DiseasesPodocytesApoptosisFemaleHumansMaleSignal TransductionSphingolipidsSphingolipidsglomerular diseasessphingolipidstubulointerstitial diseases

Identifiers

PMID35457062
PMCPMC9025012
OpenAlexW4223606533

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.