Fig. 7: Proposed outline of the signalling pathways activated in hAMSC after exposure to increasing BPA concentrations. | Cell Death Discovery

Fig. 7: Proposed outline of the signalling pathways activated in hAMSC after exposure to increasing BPA concentrations.

From: Bisphenol-A disrupts mitochondrial functionality leading to senescence and apoptosis in human amniotic mesenchymal stromal cells

Fig. 7

Alteration in mitochondrial function, evidenced by enhanced production of ROS in hAMSC after BPA exposure, trigger the downstream activation of several signalling pathways. ROS accumulation activates an antioxidant response, which is marked by an elevated production of Nrf2 and HO-1. Concurrently, the high ROS level induce sterile inflammation, resulting in increased transcription of factors involved in inflammasome complex formation and activation. However, this increased transcription does not translate to higher production of IL-1β, the downstream effector of the inflammasome pathway. Instead, oxidative stress promotes p53 stabilization and upregulates p21 and p27 genes, as well as components of the senescence-associated secretory phenotype (SASP). Ultimately, the senescent state serves as a prelude to apoptosis, which occurs when hAMSC are exposed to the highest BPA concentrations.

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