Stiffness |
Stiffness-dependent changes generally include enhanced adhesion and spreading, increased actin and cytoskeletal stiffness, increase in proliferation and migration as well as increased phagocytosis. But the connection between stiffness and macrophage phenotype remains complicated |
Surface topography |
Surface topography, such as roughness and micropatterns, can guide macrophage behavior by modifying their adhesion, spreading, elongation, and motility on the surface. Specifically, using topography design to force macrophages into elongated cell shape is shown to promote a pro-regenerative M2 phenotype |
Surface modification |
Surface modification like coating or modifying surface chemistry directly alters how macrophages engage with the material. There is a clear role for integrin-mediated regulation of macrophage migration, phagocytosis, and activation, but the precise mechanisms still remain relatively unknown |
Geometry |
Scaffold geometry affects macrophage phenotype by spatially confining macrophages and limiting their spreading, thereby leads to an alteration in actin polymerization, chromatin compaction, and epigenetic alterations |
Hemodynamic loads |
Macrophages reside within mechanically active tissues and are constantly exposed to dynamic external forces, such as stretch and cyclic strain. These forces can cause macrophages to elongate along the direction of force, therefore affecting their phenotypes. However, there is still no consensus on the mechanism of mechanical forces in influencing macrophage function |