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During the electron transfer process, a small portion of the leaked electrons can react non-enzymatically with O 2 to generate (102, 103) ( Figure 1 )

Accumulating evidence suggests that metabolic disturbances can promote the development of AF through structural and electrophysiological remodelling, but the underlying mechanisms that predispose an individual to AF are aetiology-dependent, thus emphasizing the need for tailored therapeutic strategies to treat AF that target an individuals metabolic profile

Concurrently, to reverse neurological damage, innovative strategies should be explored including glial cell reprogramming (e.g., tamoxifen derivatives inducing neuroprotective astrocytes) and microbial-mitochondrial axis interventions, combined with high-throughput screening of BBB-protective agents using organoid models

combined TME-responsive nanoprodrugs (MPNPs) with oncolytic herpes simplex virus- 1 (OVs) to enhance immunotherapy through pyroptosis induction in oral cancer cells

Roth S, Spalinger MR, Gottier C, Biedermann L, Zeitz J, Lang S