Evidence map›Paper›PMID 35616233›Full record

SynthesisJournal of cellular physiology2022

What protein kinases are crucial for acantholysis and blister formation in pemphigus vulgaris? A systematic review.

Adriano Brescacin, Zunaira Baig, Jaspreet Bhinder, Sen Lin, Lovejot Brar, Nicola Cirillo

Open access · hybridAbstract readSystematic Review
In one paragraph

Synthesis in Journal of cellular physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. 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

6 authors at 1 institution in 1 country.

Adriano BrescacinMelbourne Dental School, Faculty of Medicine, Dentistry & Health Sciences, University of Melbourne, Carlton, Victoria, Australia.
Zunaira BaigMelbourne Dental School, Faculty of Medicine, Dentistry & Health Sciences, University of Melbourne, Carlton, Victoria, Australia.
Jaspreet BhinderMelbourne Dental School, Faculty of Medicine, Dentistry & Health Sciences, University of Melbourne, Carlton, Victoria, Australia.
Sen LinMelbourne Dental School, Faculty of Medicine, Dentistry & Health Sciences, University of Melbourne, Carlton, Victoria, Australia.
Lovejot BrarMelbourne Dental School, Faculty of Medicine, Dentistry & Health Sciences, University of Melbourne, Carlton, Victoria, Australia.
Nicola CirilloMelbourne Dental School, Faculty of Medicine, Dentistry & Health Sciences, University of Melbourne, Carlton, Victoria, Australia.ORCID 0000-0003-1429-1323
The University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pemphigus vulgaris (PV) is a potentially fatal autoimmune blistering disease characterized by cell-cell detachment (or acantholysis) and blister formation. While the signaling mechanisms that associate with skin/mucosal blistering are being elucidated, specific treatment strategies targeting PV-specific pathomechanisms, particularly kinase signaling, have yet to be established. Hence, the aim of this review was to systematically evaluate molecules in the class of kinases that are essential for acantholysis and blister formation and are therefore candidates for targeted therapy. English articles from PubMed and Scopus databases were searched, and included in vitro, in vivo, and human studies that investigated the role of kinases in PV. We selected studies, extracted data and assessed risk of bias in duplicates and the results were reported according to the methodology outlined by the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA). The risk of bias assessment was performed on in vivo studies utilizing SYRCLE's risk of bias tool. Thirty-five studies were included that satisfied the pathogenicity criterion of kinases in PV, the vast majority being experimental models that used PV sera (n = 13) and PV-IgG (n = 22). Inhibition of kinase activity (p38MAPK, PKC, TK, c-Src, EGFR, ERK, mTOR, BTK, and CDK2) was achieved mostly by pharmacological means. Overall, we found substantial evidence that kinase inhibition reduced PV-associated phosphorylation events and keratinocyte disassociation, prevented acantholysis, and blocked blister formation. However, the scarce adherence to standardized reporting systems and the experimental protocols/models used did limit the internal and external validity of these studies. In summary, this systematic review highlighted the pathogenic intracellular events mediated by kinases in PV acantholysis and presented kinase signaling as a promising avenue for translational research. In particular, the molecules identified and discussed in this study represent potential candidates for the development of mechanism-based interventions in PV.

Indexed as

AcantholysisPemphigusAutoantibodiesBlisterHumansImmunoglobulin GKeratinocytesPhosphorylationAutoantibodiesImmunoglobulin Gacantholysiskinase inhibitorspemphigus vulgarisprotein kinase

Identifiers

PMID35616233
PMCPMC9540544
OpenAlexW4281565640

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.