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“Mitochondrial stabilization” refers to processes or interventions that maintain mitochondrial structure and function, primarily by regulating the balance between mitochondrial fission and fusion, ensuring adequate biogenesis, preventing pathological permeabilization of membranes, and protecting against apoptotic or necrotic cell death. Key molecular players include dynamin-related GTPases (particularly Drp1), fusion proteins (mitofusins, OPA1), anti- and pro-apoptotic BCL-2 family members, and scaffolding proteins such as AKAP1, which help localize signaling enzymes to the mitochondria.[2][3][1][4][5] Damage or dysregulation of these processes is implicated in a range of diseases including neurodegeneration, cancer, and cardiovascular pathologies, and targeting their regulation is a therapeutic area of interest, although 'mitochondrial stabilization' is not a singular drug target.”

Other names

mitochondrial integritymitochondrial quality controlmitochondrial protectionmaintenance of mitochondrial function

Inhibition of mitochondrial fission proteins to promote mitochondrial fusion/elongation (e.g., Drp1 inhibition[2][3]) - Enhancement of anti-apoptotic pathways (e.g., BCL-2 family proteins[1][4]) - Promotion of mitochondrial biogenesis and integrity through signaling pathways (e.g., cAMP/PKA/AKAP1 complex[2])