AKAP1 is a mitochondrial outer membrane-anchoring protein that coordinates compartmentalized PKA signaling to regulate diverse cellular processes. Functionally, AKAP1 binds regulatory subunits of PKA and recruits them to the mitochondrial surface, enabling spatially-localized phosphorylation events 1. Beyond its canonical scaffolding role, AKAP1 recruits electron transport chain mRNA to the outer membrane for localized translation, with loss of AKAP1 reducing ETC protein levels 2. In metabolism, AKAP1 phosphorylates and inactivates GPAT1 via PKA signaling to suppress lysophosphatidic acid synthesis, protecting against diet-induced liver steatosis 3. AKAP1 also regulates mitochondrial dynamics by maintaining Drp1 phosphorylation at inhibitory sites, preventing excessive fission 4, and controls mtDNA replication by phosphorylating Larp1, reducing TFAM expression 5. Clinically, AKAP1 dysfunction associates with multiple pathologies: upregulation impairs mtDNA replication and podocyte injury in diabetic kidney disease 5; suppression by miR-199a-5p aggravates renal ischemia-reperfusion injury 4; and dysregulation contributes to intervertebral disc degeneration 1. Additionally, AKAP1 phosphorylates GRP75 at mitochondria-associated ER membranes to protect cancer cells against ferroptosis 6. These findings position AKAP1 as a versatile signaling hub with therapeutic potential across metabolic, degenerative, and cancer-related diseases.