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Additionally, cell death and membrane damage cause an additional massive release of glutamate and ATP, aggravating the initial ischemia-induced damage (Matute and Ransom, 2012)

Mechanistically, macrophages post-MI recognize DAMPs released from necrotic cells through Toll-like receptors (TLRs), activating downstream signaling pathways such as the mTOR pathway and entering an activated state with increased energy demands (224, 226)