Is clonal haematopoiesis the missing link between lupus and cardiovascular disease?

Authors

Aamir Shamsi, Chris Wincup, Charis Pericleous, Fareeha Tariq, Matthew Sadler, Lynn Quek, Daniel Bromage

Published in

Rheumatology (Oxford, England). Jun 25, 2026. Epub Jun 25, 2026.

Abstract

Systemic lupus erythematosus (SLE) is an established, independent risk factor for cardiovascular disease (CVD), most notably premature atherosclerotic cardiovascular disease (ASCVD). This association is thought to relate to chronic immune mediated inflammation. Clonal expansion of haematopoietic stem and progenitor cells (HSPCs) with acquired mutations, but no evidence of a blood disorder, is known as clonal haematopoiesis of indeterminate potential (CHIP). CHIP is associated with a pro-inflammatory immune phenotype, driven predominantly by mutant myeloid cells, and is similarly strongly associated with ASCVD. When SLE and CHIP co-occur, there may be synergy of their canonical cellular and molecular inflammatory pathways or even convergence of pathways through shared mechanisms of immune dysregulation, which accelerate CVD. Furthermore, enrichment of HSPC clones carrying CHIP driver mutations has been observed in chronic inflammatory conditions, including SLE. In this review, we explore the emerging role of CHIP in the relationship between SLE and ASCVD, proposing it as a pathogenic nexus in a triangular inflammatory network. Defining these relationships will help early identification of high-risk individuals and facilitate therapeutic targeting of CHIP to mitigate ASCVD complications in SLE patients.

PMID:
42348225
Bibliographic data and abstract were imported from PubMed on 25 Jun 2026.

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