Evidence map›Paper›PMID 42082285›Full record

ArticleRMD open2026

Heat-not-burn tobacco induces protein post-translational modifications and apoptosis in bronchial cells: possible role in rheumatoid arthritis.

Claudia Ciancarella, Federica Maria Ucci, Valeria Manganelli, Tina Garofalo, Elena Fasciolo, Roberta Priori, Fulvia Ceccarelli, Manuel Sergi, Camilla Montesano, Francesco Bartolini and 4 more

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Article in RMD open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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No citing paper in PubMed yet.

4 · The record

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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.

Claudia Ciancarella *Department of Medical and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy claudia.ciancarella@uniroma1.it.ORCID 0009-0007-3358-5606
Federica Maria Ucci *Department of Medical and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Valeria Manganelli *Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Tina GarofaloInterdisciplinary Department of Wellbeing, Health and Environmental Sustainability, Sapienza University of Rome, Rome, Italy.
Elena FascioloDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Roberta PrioriDepartment of Medical and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Fulvia CeccarelliDepartment of Medical and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Manuel SergiDepartment of Chemistry, Sapienza University of Rome, Rome, Italy.
Camilla MontesanoDepartment of Chemistry, Sapienza University of Rome, Rome, Italy.
Francesco BartoliniDepartment of Chemistry, Sapienza University of Rome, Rome, Italy.
Antonio Sili ScavalliDepartment of Medical and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Fabrizio ContiDepartment of Medical and Cardiovascular Sciences, Sapienza University of Rome, Rome, Italy.
Maurizio SoriceDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Cristiano AlessandriInterdisciplinary Department of Wellbeing, Health and Environmental Sustainability, Sapienza University of Rome, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesSmoking is recognised as one of the strongest environmental risk factors for the development of rheumatoid arthritis (RA). Cigarette smoke increases protein post-translational modifications (PTMs), including citrullination and carbamylation, involved in the pathogenetic mechanisms of RA. Recently, tobacco companies developed new products, such as iQOS, a heat-not-burn cigarette (HNBC), which are becoming increasingly used. To date, only two epidemiological studies have been conducted in the rheumatology field. However, no studies are available on the effects of HNBCs on the pathogenic mechanisms involved in rheumatic diseases. We aimed to evaluate whether HNBCs are associated with an increase in PTMs and their effects on cell death mechanisms, such as apoptosis.

methodsHuman bronchial cells (BEAS-2B) were treated with cigarette smoke extracts from traditional cigarettes (TC) and HNBC. Western blot was performed to assess protein citrullination and carbamylation, while apoptosis was assessed by flow cytometry, after staining with annexin V-FITC/PI and western blot through enzyme Parp1 evaluation.

resultsThe exposure of BEAS-2B to HNBC or TC extracts causes significantly increased citrullination and carbamylation of proteins, compared with untreated cells. Furthermore, it leads to an augmentation of apoptosis, evaluated through annexin V-FITC/PI and enzyme Parp1 levels.

conclusionOur results show that the extracts of HNBC and TC increase citrullination, carbamylation and influence cell death, causing an activation of apoptosis. This is the first study showing the effects of HNBC on PTMs and cell death mechanisms, raising alarm about the safety of these smoking alternatives in rheumatology. These data allow us to speculate that HNBC, like TC, could represent a risk factor for the development of RA in genetically susceptible individuals.

Indexed as

ApoptosisArthritis, RheumatoidBronchiProtein Processing, Post-TranslationalCell LineCitrullinationHumansProtein CarbamylationSmokingAutoantibodiesPublic HealthRheumatoid ArthritisSmoking

Identifiers

PMID42082285
PMCPMC13141111

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