The fat tissue surrounding major arteries may hold the key to preventing strokes caused by unstable arterial plaques. This discovery challenges the traditional view that perivascular adipose tissue is merely passive padding around blood vessels, revealing instead that it actively participates in the dangerous remodeling that leads to stroke-causing blockages.
Analysis of tissue samples from 169 patients revealed two distinct populations of adipose-derived stem cells within perivascular fat that directly contribute to plaque instability. CD55-positive stem cells migrate from surrounding fat into arterial plaques, where they transform into endothelial cells and secrete FGF2 protein. This process drives pathological blood vessel formation within plaques—a hallmark of unstable lesions prone to rupture. A second population marked by CXCL14 expression worsens inflammation by recruiting immune cells through the CXCL12-CXCR4 signaling pathway. Patients with symptomatic carotid stenosis or previous stroke showed elevated levels of CD55-positive cells.
This finding represents a paradigm shift in understanding atherosclerosis progression. Rather than focusing solely on lipid accumulation and immune responses within vessel walls, researchers must now consider how adjacent fat tissue actively destabilizes plaques. The identification of CD55 as a surface marker opens potential therapeutic avenues—targeting these specific stem cell populations could prevent plaque rupture without broad immunosuppression. However, the research remains observational, and translating these cellular insights into clinical interventions will require extensive safety testing. The complexity of the perivascular microenvironment suggests that therapeutic approaches must carefully balance preventing harmful stem cell migration while preserving beneficial fat tissue functions.