Why the study?
Studies have increasingly linked NMIIA activity to diseases beyond MYH9-related disorders, including cancer, neurological diseases, and infectious disorders.
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Design
Systematic review
MYH9 mutations' links to macrothrombocytopenia and complications remain hypothesis-generating; leaves open targeted research in affected patients.
The MYH9 gene encodes the heavy chain of non-muscle myosin IIA (NMIIA), which converts chemical energy into mechanical energy and provides power for the contraction of the actin cytoskeleton. This is necessary for many important physiological processes such as cell morphology maintenance, migration, adhesion, division and individual development. Patients with autosomal dominant genetic diseases caused by MYH9 mutation show macrothrombocytopenia and complications such as renal failure, deafness and cataracts. However, in recent years, more and more studies have found that the activity of NMIIA is also related to various other diseases, including cancer, neurological diseases and infectious disorders. This article introduces the characteristics of myosin superfamily members and systematically reviews the structure, regulation and physiological functions of MYH9 and NMIIA, as well as MYH9-related disorders (MYH9-RD) caused by MYH9 mutations, focusing on the role of NMIIA in the pathogenesis of various cancers, and summarizes the therapeutic mechanisms of its targeted drugs. Besides, the effects of NMIIA in neurological diseases and infectious diseases are discussed to provide a comprehensive theoretical basis and insights for MYH9 and NMIIA as a therapeutic target for multiple diseases.
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Tian et al. (2025) studied this question.
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