Abstract Body: Despite effective lipid-lowering therapies, substantial residual cardiovascular risk remains, underscoring the need to define mechanisms that promote plaque stabilization during LDL-lowering-induced atherosclerosis remodeling. Stable plaques are characterized by fibrous cap thickening and extracellular matrix remodeling, processes largely attributed to macrophages and smooth muscle cells. Whether fibroblasts directly contribute to plaque stabilization during remodeling remains unclear. Using single-cell RNA sequencing in an LDL-lowering–induced lesion remodeling mouse model with smooth muscle cell lineage tracing (ROSA26 ZsGreen1^+/+; Ldlr^−/−; Myh11-CreERT2), we identified fibroblast subpopulations that expand markedly during remodeling, revealing an unexpected role for fibroblasts in plaque stabilization. Among these, a Pi16_CD26 fibroblast population localized to the fibrous cap and was enriched for collagen biosynthesis and extracellular matrix remodeling programs consistent with a reparative phenotype. To define the regulatory mechanisms sustaining this reparative fibroblast program, we performed integrative regulatory network analysis and identified Krüppel-like factor 3 (Klf3) as a top transcriptional regulator selectively active in Pi16_CD26 fibroblasts. Loss of KLF3 function in cultured mouse and human aortic fibroblasts impaired proliferation and migration and reduced extracellular matrix gene expression, indicating disruption of the reparative fibroblast program. Together, these findings identify fibroblasts as active contributors to plaque stabilization during atherosclerosis remodeling and establish KLF3 as a central regulator maintaining a reparative fibroblast subtype transcriptional programs. This work defines a previously underappreciated stromal mechanism of plaque stabilization and highlights fibroblast-specific regulatory pathways as potential targets to reduce residual cardiovascular risk.