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used a microfluidics-based aorta smooth muscle-on-a-chip model to show that mitochondrial fusion activators or fission inhibitor can partially rescue the disorders of mitochondrial dynamics in human aorta smooth muscle cells derived from patients with the potential to develop thoracic aortic aneurysms due to a bicuspid aortic valve ( 3.2 Role of models in drug discovery and development The development of effective therapeutics for mitochondrial diseases relies heavily on the insights gained from preclinical models

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doi: 10.1111/anu.2011.17.issue-2 210 WangY