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STIM2 is, therefore, a crucial regulator of SOCE in cortical neurons, and targeting STIM2 could be a viable therapeutic strategy for reducing calcium dysregulation and subsequent mitochondrial dysfunction after TBI (Rao et al., 2015)

According to their study, the culturing of mouse vibrissae in medium containing adenoviral-Wnt10b grew faster as compared to that cultured in control medium or medium containing Wnt signaling antagonists

Further, we discuss the involvement of microglia and astrocytes in lesion formation and organization, remyelination, synaptic induction and pruning through different signaling pathways

However, these procedures are not only ineffective in the long term but also exhibit inherent issues such as limited spinal motion and accelerated degeneration of adjacent intervertebral discs

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