Smoking 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.
Keywords: Autoantibodies, Public Health, Rheumatoid Arthritis, Smoking
RMD open
Journal Article
English
42082285
Guideline Central and select third party use “cookies” on this website to enhance the user experience.
This technology helps us gather statistical and analytical information to optimize the relevant content for you.
The user also has the option to opt-out which may have an effect on the browsing experience.