PSR Activators

In the realm of cellular homeostasis, the phosphatidylserine receptor (PSR) plays a crucial role in identifying and facilitating the clearance of apoptotic cells. The activation of PSR is inherently linked to the presence of apoptotic cells; thus, compounds that induce apoptosis indirectly augment the number of targets for PSR, leading to its theoretical activation. Chemicals like Sanguinarine and Piperlongumine increase intracellular reactive oxygen species, triggering cell death pathways and enhancing PSR-mediated phagocytosis by increasing the 'eat-me' signal through phosphatidylserine exposure. Similarly, Arsenic trioxide and Withaferin A can promote apoptosis in certain cell lines, which could lead to an upsurge in PSR activity due to a higher availability of apoptotic cells.

Betulinic acid, Ursolic acid, and Capsaicin are additional examples that induce apoptosis through various intracellular mechanisms, including the mitochondrial pathway and DNA damage, leading to PSR activation. Paclitaxel, through its action on microtubules, and Thapsigargin, via calcium dysregulation, also result in apoptosis, subsequently increasing the substrates for PSR engagement. Camptothecin's inhibition of DNA topoisomerase I, Curcumin's multi-targeted apoptotic induction, and Resveratrol's pro-apoptotic effects in specific cell lines, all contribute to the heightened activation of PSR. These compounds, by amplifying the apoptotic process, could serve as indirect activators of PSR, enhancing its critical function in maintaining cellular equilibrium. The exploration of such indirect activators is predicated on the intricate balance of cell death and clearance, where PSR serves as a sentinel for phagocytic signaling.