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. Author manuscript; available in PMC: 2020 Mar 30.
Published in final edited form as: Annu Rev Pathol. 2019 Nov 5;15:419–438. doi: 10.1146/annurev-pathmechdis-012419-032544

Figure 2.

Figure 2

Central overview of age-related clonal hematopoiesis and how it drives cardiovascular disease progression. During the aging process, healthy hematopoietic stem cells (HSCs) may acquire a mutation in a driver gene. This mutation provides the mutant HSC with a competitive advantage, allowing for its expansion at a disproportionate rate compared with other HSCs within the bone marrow niche (clonal expansion). As a result, the HSC-derived mutation propagates through the hematopoietic system and into its immediate leukocyte progeny, giving rise to a genetically distinct population of mature white blood cells. During cardiovascular disease, inflammatory cells migrate to the injury site and are involved in promoting disease pathogenesis through a variety of mechanisms. In the setting of clonal hematopoiesis, HSC-derived mutations may result in changes to the inflammatory profile of the leukocyte progeny(i.e., elevated cytokine production). As a result, this altered inflammatory profile of leukocytes can exacerbate cardiovascular injury processes, driving disease progression.