Targeting TNF-α was found to be helpful in alleviating inflammation. With TNF-α being a master regulator of inflammation, drugs that target TNF-α can help treat many diseases such as cancer and cardiovascular diseases, where TNF-α plays a critical role. Currently, anti-TNF-α drugs are not approved for treating vascular restenosis. This review article highlights the specific role of TNF-α in promoting proliferation, migration, phenotype switch, and cellular processes in vascular smooth muscle cells, which are the basis for restenosis. Molecular pathways and other mediators associated with TNF-α-induced mechanisms are discussed, which may help to develop a better strategy to use TNF-α antagonists for the treatment of restenosis.

TNF-α functions as a master regulator of inflammation, and it plays a prominent role in several immunological diseases. By promoting important cellular mechanisms, such as cell proliferation, migration, and phenotype switch, TNF-α induces its exacerbating effects, which are the underlying cause of many proliferative diseases such as cancer and cardiovascular disease. TNF-α primarily alters the immune component of the disease, which subsequently affects normal functioning of the cells. Monoclonal antibodies and synthetic drugs that can target TNF-α and impair its effects have been developed and are currently used in the treatment of a few select human diseases. Vascular restenosis is a proliferative disorder that is initiated by immunological mechanisms. In this review, the role of TNF-α in exacerbating restenosis resulting from neointimal hyperplasia, as well as molecular mechanisms and cellular processes affected or induced by TNF-α, are discussed. As TNF-α-targeting drugs are currently not approved for the treatment of restenosis, the summation of the topics discussed here is anticipated to provide information that can emphasize on the use of TNF-α-targeting drug candidates to prevent vascular restenosis.