Evidence map›Paper›PMID 35288362›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2022

Cell type-specific mechanistic target of rapamycin-dependent distortion of autophagy pathways in lupus nephritis.

Tiffany Caza, Chathura Wijewardena, Laith Al-Rabadi, Andras Perl

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
5.3field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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  16. CD3Frontiers in immunology · 2025
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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 3 institutions in 1 country.

Tiffany CazaArkana Laboratories, Little Rock, Arkansas.
Chathura WijewardenaDepartments of Medicine, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York.
Laith Al-RabadiDepartment of Medicine, University of Utah, Salt Lake City, Utah.
Andras PerlDepartments of Medicine, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York; Biochemistry and Molecular Biology, Neuroscience and Physiology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York; Medicine, Microbiology and Immunology, Biochemistry and Molecular Biology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York. Electronic address: perla@upstate.edu.
SUNY Upstate Medical University · USArkana Laboratories · USUniversity of Utah · US

Funding

SLE Treatment with N-acetylcysteineU01AR076092 · NIAMS · UPSTATE MEDICAL UNIVERSITY · PI Michael P McDermott, Andras Perl · 2020 to 2026
$7.9M
Metabolic Control of T-cell Lineage Specification in SLER01AI072648 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2008 to 2024
$6.1M
IMPACT OF HRES-1 ENDOGENOUS RETROVIRUS IN SLER01AI048079 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2000 to 2013
$2.7M
Endocytic Control of Autophagosome Formation in Lupus T cellsR01AI122176 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2016 to 2020
$2.0M
Treatment of SLE with sirolimusR34AI141304 · NIAID · UPSTATE MEDICAL UNIVERSITY · PI PERL, ANDRAS · 2019 to 2019
$243k
NIAID NIH HHS R01 AI048079NIAID NIH HHS R01 AI072648NIAID NIH HHS R01 AI122176NIAID NIH HHS R34 AI141304NIAMS NIH HHS U01 AR076092
6 · The paper itself

Abstract

Pro-inflammatory immune system development, metabolomic defects, and deregulation of autophagy play interconnected roles in driving the pathogenesis of systemic lupus erythematosus (SLE). Lupus nephritis (LN) is a leading cause of morbidity and mortality in SLE. While the causes of SLE have not been clearly delineated, skewing of T and B cell differentiation, activation of antigen-presenting cells, production of antinuclear autoantibodies and pro-inflammatory cytokines are known to contribute to disease development. Underlying this process are defects in autophagy and mitophagy that cause the accumulation of oxidative stress-generating mitochondria which promote necrotic cell death. Autophagy is generally inhibited by the activation of the mammalian target of rapamycin (mTOR), a large protein kinase that underlies abnormal immune cell lineage specification in SLE. Importantly, several autophagy-regulating genes, including ATG5 and ATG7, as well as mitophagy-regulating HRES-1/Rab4A have been linked to lupus susceptibility and molecular pathogenesis. Moreover, genetically-driven mTOR activation has been associated with fulminant lupus nephritis. mTOR activation and diminished autophagy promote the expansion of pro-inflammatory Th17, Tfh and CD3

Indexed as

Lupus Erythematosus, SystemicLupus NephritisAutophagyEndothelial CellsHumansSirolimusTOR Serine-Threonine KinasesSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID35288362
PMCPMC9240418
OpenAlexW4221020542

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.