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Thereby, the magnitude and duration of TGF- signaling is carefully controlled at many different levels, including the synthesis and activation of latent TGF- isoforms, receptor activation and stability, and the activation and stability of intracellular Smad molecules and other downstream signaling molecules

In pathological conditions, astrocytes undergo significant molecular and morphological remodeling, adopting either a detrimental A1 (neurotoxic) or beneficial A2 (neuroprotective) reactive state that, respectively, drives injury progression or promotes tissue repair [132, 133]

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