ArticleeLife2021
Aorta smooth muscle-on-a-chip reveals impaired mitochondrial dynamics as a therapeutic target for aortic aneurysm in bicuspid aortic valve disease.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Development of a Multi-Channel and Multilayered PDMS Microfluidic Platform for Real-Time Visualization and Multi-Condition Parallel Testing of Mechanically Stimulated Cells.Micromachines · 2026Article
- Mitochondrial dynamics in neurodevelopment and neurodevelopmental disorders.Nature reviews. Neuroscience · 2026Review
- Mitochondrial cardiovascular diseases: molecular mechanisms, multi-omics exploration and therapeutic strategies.Journal of advanced research · 2026Review
- Interplay between acute Type A aortic dissection and pan-cancer: Clinical evidence, bioinformatics, and experimental validation.iScience · 2025Article
- Biomechanical research using advanced micro-nano devices: In-Vitro cell Characterization focus.Journal of advanced research · 2025Review
- Measurement of oxygen consumption rate in mouse aortic tissue.Biology methods & protocols · 2025Article
- Circulating PGC-1α and MOTS-c Peptide as Potential Mitochondrial Biomarkers in Patients Undergoing Aortic Valve Replacement.Biologics : targets & therapy · 2025Article
- Preclinical models of mitochondrial dysfunction: mtDNA and nuclear-encoded regulators in diverse pathologies.Frontiers in aging · 2025Review
- Ciprofloxacin Accelerates Angiotensin-II-Induced Vascular Smooth Muscle Cells Senescence Through Modulating AMPK/ROS pathway in Aortic Aneurysm and Dissection.Cardiovascular toxicology · 2024Article
- Mitochondrial dysfunction: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- Addressing Cardiovascular Toxicity Risk of Electronic Nicotine Delivery Systems in the Twenty-First Century: "What Are the Tools Needed for the Job?" and "Do We Have Them?"Cardiovascular toxicology · 2024Review
- Utilization of an Artery-on-a-Chip to Unravel Novel Regulators and Therapeutic Targets in Vascular Diseases.Advanced healthcare materials · 2024Article
- Mitochondrial influences on smooth muscle phenotype.American journal of physiology. Cell physiology · 2024Review
- Understanding genomic medicine for thoracic aortic disease through the lens of induced pluripotent stem cells.Frontiers in cardiovascular medicine · 2024Review
- Mitochondrial non-energetic function and embryonic cardiac development.Frontiers in cell and developmental biology · 2024Review
- Species-specific FMRP regulation of RACK1 is critical for prenatal cortical development.Neuron · 2023Article
- Using biophysical cues and biomaterials to improve genetic models.Current opinion in biomedical engineering · 2023Article
- Mitochondrial dysfunction at the crossroad of cardiovascular diseases and cancer.Journal of translational medicine · 2023Review
- Multi-omics in thoracic aortic aneurysm: the complex road to the simplification.Cell & bioscience · 2023Review
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Bicuspid aortic valve (BAV) is the most common congenital cardiovascular disease in general population and is frequently associated with the development of thoracic aortic aneurysm (TAA). There is no effective strategy to intervene with TAA progression due to an incomplete understanding of the pathogenesis. Insufficiency of NOTCH1 expression is highly related to BAV-TAA, but the underlying mechanism remains to be clarified. Methods: A comparative proteomics analysis was used to explore the biological differences between non-diseased and BAV-TAA aortic tissues. A microfluidics-based aorta smooth muscle-on-a-chip model was constructed to evaluate the effect of NOTCH1 deficiency on contractile phenotype and mitochondrial dynamics of human aortic smooth muscle cells (HAoSMCs). Results: Protein analyses of human aortic tissues showed the insufficient expression of NOTCH1 and impaired mitochondrial dynamics in BAV-TAA. HAoSMCs with NOTCH1-knockdown exhibited reduced contractile phenotype and were accompanied by attenuated mitochondrial fusion. Furthermore, we identified that mitochondrial fusion activators (leflunomide and teriflunomide) or mitochondrial fission inhibitor (Mdivi-1) partially rescued the disorders of mitochondrial dynamics in HAoSMCs derived from BAV-TAA patients. Conclusions: The aorta smooth muscle-on-a-chip model simulates the human pathophysiological parameters of aorta biomechanics and provides a platform for molecular mechanism studies of aortic disease and related drug screening. This aorta smooth muscle-on-a-chip model and human tissue proteomic analysis revealed that impaired mitochondrial dynamics could be a potential therapeutic target for BAV-TAA. Funding: National Key R and D Program of China, National Natural Science Foundation of China, Shanghai Municipal Science and Technology Major Project, Shanghai Science and Technology Commission, and Shanghai Municipal Education Commission.
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