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. Author manuscript; available in PMC: 2023 Apr 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2022 Feb 17;42(4):372–380. doi: 10.1161/ATVBAHA.121.316233

Figure 1. Reciprocal Crosstalk between Macrophages and vSMCs.

Figure 1.

Macrophages clearing dead cells produce pro-resolving mediators, such as IL-10, TGFβ, and SPMs. These in turn cause vSMCs to differentiate and deposit ECM, leading to thicker fibrous caps. However, when efferocytosis is impaired, macrophages release pro-inflammatory mediators, such as TNFα, IL-1β, and IL-6 that cause vSMC de-differentiation, ECM degradation, and fibrous cap thinning. These functions are reciprocal and can lead to either plaque stability or rupture-prone atheromas.