DNM2 encodes dynamin 2, a GTPase that catalyzes GTP hydrolysis to mediate vesicle scission during endocytosis and actin cytoskeleton remodeling 12345. The protein self-assembles into ring-like helical polymers around vesicle membranes to facilitate clathrin-mediated endocytosis, exocytic trafficking, and macropinocytosis 134. In actin organization, DNM2 bundles filaments through interaction with cortactin (CTTN), with GTP hydrolysis triggering rapid depolymerization and actin bundle dispersal 2. DNM2 participates in autophagy by facilitating ATG9A vesicle formation and autophagosome release through interactions with SNX18 and MAP1LC3B 67. Autosomal dominant DNM2 mutations cause two distinct neuromuscular diseases: centronuclear myopathy (CNM) and dominant intermediate Charcot-Marie-Tooth neuropathy (CMT), with CNM mutations potentially causing protein hyperactivity while CMT mutations impair lipid binding 8. DNM2 upregulation modifies X-linked and autosomal recessive CNM phenotypes, and reducing DNM2 reverts muscle pathology in preclinical models 8. Additionally, DNM2 participates in macropinocytosis-associated muscle wasting in pancreatic cancer through the ZIP4/SDC1 pathway 9.