Ischemic stroke is a major cause of mor-bidity and mortality, and currently there is no effective treatment. The family of protein kinase C (PKCs) could phosphorylate serine or threonine residues of its substrate proteins and play a key role in the ischemia/reperfusion injury. Autophagy is essential for maintaining cell ho-meostasis under physiological condition and acts as a double-edged sword in the process of ischemic neuronal death. In this article, we reviewed the PKCs isoform-spe-cific signaling pathways and PKC-modulated autophagy in ischemic stroke.