Background: Cerebrovascular and cardiovascular diseases are caused by impairment
of the brain and/or heart circulation. Insufficient blood flow results in decreased oxygen
delivery (ischemia), which affects mitochondrial functioning and consequently leads to insufficient
ATP production. The predominant mitochondrial outer membrane protein, the voltagedependent
anion selective channel (VDAC), is considered to be crucial for mitochondrial
functioning. In human mitochondria, as in other vertebrates, three isoforms of VDAC
(VDAC1-VDAC3) are present, and they likely play different roles.
Objective: In this review, we summarize the available data concerning VDAC involvement in
cardiovascular and cerebrovascular diseases with regard to VDAC isoforms and discuss the use
of possible VDAC-related intervention targets as well as known VDAC-interacting and cytoprotection-
conferring molecules in the treatment of cerebrovascular and cardiovascular diseases.
Method and Results: The suitable references on disorders defined as cerebrovascular and cardiovascular
diseases as well as VDAC contribution to these conditions were searched using PubMed
and ClinicalTrials.gov databases. The review is based on the 138 carefully selected articles.
Conclusion: Mitochondrial dysfunction triggered by changes in VDAC properties undoubtedly
contributes to cell death and related diseases, including cerebrovascular and cardiovascular
diseases. Thus, beside diagnostic application, modulation of VDAC activity, including its
isoforms, is thus of great importance for the development of efficient therapeutic interventions.
Moreover, identification of VDAC-interacting molecules that protect against mitochondrial
dysfunction and cell death seems to be of great importance.