Figure 8.

Schematic representation of the proposed mechanisms by which melatonin protects against ER stress/autophagy‐induced cell death through upregulation of the cellular prion protein (PrP^C) levels. Treatment of MSCs with melatonin inhibits ER stress, autophagy and apoptosis via PrP^C upregulation. Moreover, melatonin increases the activation of MnSOD and catalase activity. Transplantation of melatonin‐treated MSCs improves the functional recovery and vessel formation in ischaemic diseases through this melatonin‐mediated PrP^C expression