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Its mechanism is understood as potassium-channel opening and vasodilation, with prolongation of the anagen growth phase

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In this manuscript, we propose that an integrative neurogenomics workflowcombining multi-omic phenotypeoriented whole-exome sequencing, biologically-oriented common variant burden profiling, biochemical markers, functional metagenomic data, and multidisciplinary clinical interpretationcan generate testable, personalized diagnostic and therapeutic hypotheses in neurodegenerative disorders

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This outcome might be linked to the triggering of F-actin formation, as indicated by FITC-phalloidin staining