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Such dynamic changes highlight the importance of tightly maintained astrocytic Cl− homeostasis for supporting normal neuronal function, especially under prolonged or repetitive bouts of synaptic activation and inhibition

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Notably, the recognition of limited or partial EndoMT does not necessarily conflict with its potential functional relevance in PA stiffening, but simply suggests that this relevance may potentially relate more to the release of proliferative, hypertrophic, and profibrotic signals—i.e., mediators of processes that will ultimately promote PA stiffness—by partial EndoMT cells rather than to the actual generation of significant mesenchymal cell mass via this mechanism