| Autor: |
Boosani CS; Somatic Cell and Genome Editing Center, Division of Animal Science, College of Agriculture Food and Natural Resources, University of Missouri, Columbia, MO 65211, USA.; MU HealthCare, University of Missouri, Columbia, MO 65211, USA.; Technology and Platform Development, Soma Life Science Solutions, Winston-Salem, NC 27103, USA., Burela L; Aurora's Degree and PG College, Chikkadpally, Hyderabad 500020, India. |
| Jazyk: |
angličtina |
| Zdroj: |
Cancers [Cancers (Basel)] 2024 Apr 08; Vol. 16 (7). Date of Electronic Publication: 2024 Apr 08. |
| DOI: |
10.3390/cancers16071435 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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