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These distinct mechanisms may include systemic dysfunction-induced neurologic injury, renin-angiotensin system (RAS) dysfunction, immune dysfunction, and direct viral invasion of the nervous system, as elaborated and summarized in Table 1 [55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71] and Fig

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239 Elevated expression of ATG genes, including ATG4B, ATG4D, ATG5, and BECN1, underscores its mechanistic relevance, 240 and ATG4B knockdown sensitizes cells to therapy

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