Why the study?
The pathogenesis of rheumatoid arthritis is complex and not fully elucidated, including extra-articular manifestations and increased cardiovascular risk.
This review provides an overview of recent insights into the pathogenesis of rheumatoid arthritis, highlighting immune mechanisms and associated cardiovascular risk.
Elevated CV risk in RA warrants clinical vigilance; leaves open mechanistic targets for prospective trials.
The pathogenesis of rheumatoid arthritis (RA) is a complex scenario that, to date, is not fully elucidated. However, scientific progress has enabled us to understand several mechanisms underlying the development of the disease. The breakdown of self-tolerance in genetically predisposed individuals and the aberrant activation of innate and adaptive immune responses culminate in synovial hyperplasia and bone destruction. In addition, extra-articular manifestations, as well as the burden of increased cardiovascular risk (CVR), in patients with RA represent another interesting aspect of RA pathogenesis under intense investigation. The purpose of this review article is to provide an overview of the new insights in RA pathogenesis summarising the most relevant studies published over the last year.
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Testa et al. (2021) studied this question.
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