Technical Articles

This article focuses on the central role of Activin A in tumor immune evasion, systematically elucidating the molecular mechanisms by which this cytokine suppresses the proliferation and activity of natural killer cells to weaken anti-tumor immune responses, and analyzing the therapeutic potential of targeting Activin A to restore NK cell function.

This article systematically elucidates the central role of Activin A in the development and progression of cancer cachexia, focusing on the molecular mechanism by which this cytokine drives skeletal muscle atrophy through inhibiting PGC1α expression in vascular endothelial cells and inducing endothelial dysfunction.

Activin A, a key member of the TGF-β superfamily, is a dimeric protein formed by two βA subunits linked via disulfide bonds. This critical signaling molecule plays a central role in physiological processes such as embryonic development, tissue repair, and immune regulation, but its dysregulation has also become a pivotal factor in the pathogenesis of various diseases.

Activin A is a secreted protein belonging to the transforming growth factor-β superfamily. Like other well-known family members such as TGF-β and BMPs, it plays a central role in cell growth, differentiation, and apoptosis.