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. Author manuscript; available in PMC: 2024 Oct 1.
Published in final edited form as: Mech Ageing Dev. 2023 Sep 1;215:111859. doi: 10.1016/j.mad.2023.111859

Figure 6: A proposed schematic of the role of PRDX3 and PRDX4 in aged hearts.

Figure 6:

A deficiency of PRDX4 is a potential mechanism of the increase in the ER stress that occurs during aging by augmenting oxidative stress. An increase in ER stress leads to mitochondrial dysfunction and PRDX3 defects during aging by activating mitochondrial calpain 1 (CPN1) (Chen et al., 2022b; Thompson et al., 2020). The 4-PBA treatment improves mitochondrial function and PRDX3 content by decreasing the ER stress that in turn attenuates the activation of mitochondrial calpain 1 (Chen et al., 2020; Chen et al., 2022b). Restoration of PRDX4 content is another potential strategy to decrease the ER stress during aging.