Evidence map›Paper›PMID 30429845›Full record

ReviewFrontiers in immunology2018

Potential Role of Cytochrome c and Tryptase in Psoriasis and Psoriatic Arthritis Pathogenesis: Focus on Resistance to Apoptosis and Oxidative Stress.

Maria Sole Chimenti, Flavia Sunzini, Laura Fiorucci, Elisabetta Botti, Giulia Lavinia Fonti, Paola Conigliaro, Paola Triggianese, Luisa Costa, Francesco Caso, Alessandro Giunta and 4 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

49 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
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  6. Article
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  8. Article
  9. Review
  10. Article
  11. Dialogue between programmed cell death and psoriasis.Postepy dermatologii i alergologii · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Redox Pathogenesis in Rheumatic Diseases.ACR open rheumatology · 2024
    Review
  17. Review
  18. Article
  19. Review
  20. Article
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

14 authors at 2 institutions in 1 country.

Maria Sole ChimentiRheumatology, Allergology and Clinical Immunology, University of Rome Tor Vergata, Rome, Italy.
Flavia SunziniRheumatology, Allergology and Clinical Immunology, University of Rome Tor Vergata, Rome, Italy.
Laura FiorucciDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome, Italy.
Elisabetta BottiDermatology, University of Rome Tor Vergata, Rome, Italy.
Giulia Lavinia FontiRheumatology, Allergology and Clinical Immunology, University of Rome Tor Vergata, Rome, Italy.
Paola ConigliaroRheumatology, Allergology and Clinical Immunology, University of Rome Tor Vergata, Rome, Italy.
Paola TriggianeseRheumatology, Allergology and Clinical Immunology, University of Rome Tor Vergata, Rome, Italy.
Luisa CostaRheumatology Unit, Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy.
Francesco CasoRheumatology Unit, Department of Clinical Medicine and Surgery, University of Naples Federico II, Naples, Italy.
Alessandro GiuntaDermatology, University of Rome Tor Vergata, Rome, Italy.
Maria EspositoDermatology, University of Rome Tor Vergata, Rome, Italy.
Luca BianchiDermatology, University of Rome Tor Vergata, Rome, Italy.
Roberto SantucciDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, Rome, Italy.
Roberto PerriconeRheumatology, Allergology and Clinical Immunology, University of Rome Tor Vergata, Rome, Italy.
University of Rome Tor Vergata · ITUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis (PsO) is an autoimmune disease characterized by keratinocyte proliferation, chronic inflammation and mast cell activation. Up to 42% of patients with PsO may present psoriatic arthritis (PsA). PsO and PsA share common pathophysiological mechanisms: keratinocytes and fibroblast-like synoviocytes are resistant to apoptosis: this is one of the mechanism facilitating their hyperplasic growth, and at joint level, the destruction of articular cartilage, and bone erosion and/or proliferation. Several clinical studies regarding diseases characterized by impairment of cell death, either due to apoptosis or necrosis, reported cytochrome c release from the mitochondria into the extracellular space and finally into the circulation. The presence of elevated cytochrome c levels in serum has been demonstrated in diseases as inflammatory arthritis, myocardial infarction and stroke, and liver diseases. Cytochrome c is a signaling molecule essential for apoptotic cell death released from mitochondria to the cytosol allowing the interaction with protease, as the apoptosis protease activation factor, which lead to the activation of factor-1 and procaspase 9. It has been demonstrated that this efflux from the mitochondria is crucial to start the intracellular signaling responsible for apoptosis, then to the activation of the inflammatory process. Another inflammatory marker, the tryptase, a trypsin-like serine protease produced by mast cells, is released during inflammation, leading to the activation of several immune cells through proteinase-activated receptor-2. In this review, we aimed at discussing the role played by cytochrome c and tryptase in PsO and PsA pathogenesis. To this purpose, we searched pathogenetic mechanisms in PUBMED database and review on oxidative stress, cytochrome c and tryptase and their potential role during inflammation in PsO and PsA. To this regard, the cytochrome c release into the extracellular space and tryptase may have a role in skin and joint inflammation.

Indexed as

AnimalsApoptosisArthritis, PsoriaticAutoimmunityCytochromes cHumansOxidative StressPsoriasisTryptasesCytochromes cTryptasesapoptosisautoimmunitycytochrome c and tryptaseoxidative stresspsoriatic arthritispsoriatic disease

Identifiers

PMID30429845
PMCPMC6220124
OpenAlexW2899087954

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.