Metalloendopeptidase OMA1, mitochondrial (OMA1)

Metalloendopeptidase OMA1, mitochondrial (abbreviation: OMA1), is a Zn-dependent metalloprotease located in the inner mitochondrial membrane[1][9]. It is part of the mitochondrial quality control system and is activated in response to diverse mitochondrial stresses, including loss of membrane potential and oxidative damage, where it cleaves several substrates such as the dynamin-like GTPase OPA1 and the stress signaling protein DELE1[1][2]. OMA1-mediated OPA1 cleavage is associated with mitochondrial fragmentation and the initiation of apoptosis[1]. OMA1 activation is important for adaptive stress response, prevention of reactive oxygen species accumulation, and maintenance of mitochondrial function[2]. Dysfunction or aberrant regulation of OMA1 has been associated with neurodegeneration, heart failure, cancer, and other metabolic and degenerative diseases, mostly through its influence on OPA1 and DELE1 but also possibly by other mechanisms[1]. There are currently no drugs or established biomarkers directly targeting OMA1, and its manipulation poses potential safety concerns related to mitochondrial and cellular homeostasis[1][2].

Other names

OMA1 zinc metallopeptidaseOMA1 proteaseOMA1 mitochondrialOMA1OMA1 gene product

Proteolytic cleavage of OPA1 and DELE1 in response to mitochondrial stress, triggers apoptosis or integrated stress response; general stress-activated mitochondrial quality control