Table 1.

Cell types and their role in ISR.

Cell Type	Role in ISR	Mechanism/Effect
Smooth muscle cells	Primary contributors to neointimal hyperplasia	Proliferate and migrate, contributing to luminal narrowing; transition from contractile to synthetic phenotype.
Platelets	Initial responders to stent placement	Release thromboxane A2 and PDGF, inducing oxidative stress and smooth muscle cell transition.
Mast cells	Role in neointimal formation	Release chymase, influencing angiotensin II and TGF-β production, leading to fibroblast proliferation.
Monocytes	Involved in the inflammatory response and late ISR risk	Elevated levels post-PCI are indicative of late ISR risk. Participate in cytokine secretion.
Eosinophils	Associated with late ISR	Elevated levels post-PCI are predictive of late ISR.
Macrophages	Part of the inflammatory response	Infiltrate subendothelial space, involved in neo-atherosclerosis and neointimal formation.
Endothelial cells	Affected by stent deployment	Disruption leads to exposure of the intimal layer and a prothrombotic effect.
Bone marrow progenitor cells (BMPCs)	Contribute to neointimal formation	Recruitment and proliferation within the extracellular matrix.
Fibroblasts	Involved in neointimal formation	Proliferation influenced by mast cell-released chymase and TGF-β.