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Particularly noteworthy is the finding that genetic polymorphisms of complement components C4A and C4B are significantly associated with various microbial environmental variables in schizophrenia patients, including a history of pathogen exposure and gut ecological imbalance (143)

These findings suggest that while FOXO4 is involved in the senescence pathway, it also plays a role in maintaining the viability of senescent Leydig cells by suppressing their apoptotic response, which could contribute to the accumulation of senescent cells [1]

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