ArticleCell & bioscience2022
Ubiquitinated AIF is a major mediator of hypoxia-induced mitochondrial dysfunction and pulmonary artery smooth muscle cell proliferation.
Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- The Role of Piezo Ion Channels in Pulmonary Hypertension.Pulmonary circulation · 2026Review
- Emerging significance of E3 ubiquitin ligases and Deubiquitinases in pulmonary hypertension.Molecular medicine (Cambridge, Mass.) · 2026Review
- Nicotinamide phosphoribosyltransferase activates the mitochondrial unfolded protein response to promote pulmonary arterial endothelial cell proliferation.bioRxiv : the preprint server for biology · 2026Article
- Super enhancer-driven LINC01013 mediates hypoxia-induced mitochondrial dysfunction by HSPA9 to determine pulmonary arterial smooth muscle cell fate.Cellular and molecular life sciences : CMLS · 2026Article
- Competitive Binding of UBA52 and HOPX Modulates β-catenin Stability in Colorectal Cancer in the Context of High-Iron Intake.International journal of biological sciences · 2026Article
- VDAC1: The mitochondrial gatekeeper in the battle against hearing loss (Review).Biomedical reports · 2025Review
- Osteoarthritis: Mechanisms and Therapeutic Advances.MedComm · 2025Review
- Metabolic Disturbances Involved in Cardiovascular Diseases: The Role of Mitochondrial Dysfunction, Altered Bioenergetics and Oxidative Stress.International journal of molecular sciences · 2025Review
- Transcription factor EB improves hypoxic pulmonary hypertension in fetal rats by suppressing NLRP3 inflammasome activation via induction of mitophagy.Scientific reports · 2025Article
- Multidimensional study on mitochondrial dysfunction in pulmonary hypertension.Frontiers in medicine · 2025Review
- PI3K p85α/HIF-1α accelerates the development of pulmonary arterial hypertension by regulating fatty acid uptake and mitophagy.Molecular medicine (Cambridge, Mass.) · 2024Article
- CircPMS1 promotes proliferation of pulmonary artery smooth muscle cells, pulmonary microvascular endothelial cells, and pericytes under hypoxia.Animal models and experimental medicine · 2024Article
- OPN silencing reduces hypoxic pulmonary hypertension via PI3K-AKT-induced protective autophagy.Scientific reports · 2024Article
- TUFM in health and disease: exploring its multifaceted roles.Frontiers in immunology · 2024Review
- Mitochondria in hypoxic pulmonary hypertension, roles and the potential targets.Frontiers in physiology · 2023Review
- Effect of prolactin on cytotoxicity and oxidative stress in ovine ovarian granulosa cells.PeerJ · 2023Article
- Silencing TUFM Inhibits Development of Monocrotaline-Induced Pulmonary Hypertension by Regulating Mitochondrial Autophagy via AMPK/mTOR Signal Pathway.Oxidative medicine and cellular longevity · 2022Article
- Mitochondrial dysfunction in pulmonary arterial hypertension.Frontiers in physiology · 2022Review
- The prognostic value and clinical significance of mitophagy-related genes in hepatocellular carcinoma.Frontiers in genetics · 2022Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
backgroundExcessive proliferation of pulmonary artery smooth muscle cells (PASMCs) is the main cause of hypoxic pulmonary hypertension (PH), and mitochondrial homeostasis plays a crucial role. However, the specific molecular regulatory mechanism of mitochondrial function in PASMCs remains unclear.
methodsIn this study, using the CCK8 assay, EdU incorporation, flow cytometry, Western blotting, co-IP, mass spectrometry, electron microscopy, immunofluorescence, Seahorse extracellular flux analysis and echocardiography, we investigated the specific involvement of apoptosis-inducing factor (AIF), a mitochondrial oxidoreductase in regulating mitochondrial energy metabolism and mitophagy in PASMCs.
resultsIn vitro, AIF deficiency in hypoxia leads to impaired oxidative phosphorylation and increased glycolysis and ROS release because of the loss of mitochondrial complex I activity. AIF was also downregulated and ubiquitinated under hypoxia leading to the abnormal occurrence of mitophagy and autophagy through its interaction with ubiquitin protein UBA52. In vivo, treatment with the adeno-associated virus vector to overexpress AIF protected pulmonary vascular remodeling from dysfunctional and abnormal proliferation.
conclusionsTaken together, our results identify AIF as a potential therapeutic target for PH and reveal a novel posttranscriptional regulatory mechanism in hypoxia-induced mitochondrial dysfunction.
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