ArticleScientific reports2020
p32/C1QBP regulates OMA1-dependent proteolytic processing of OPA1 to maintain mitochondrial connectivity related to mitochondrial dysfunction and apoptosis.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 38 citations in OpenAlex.
- Trained Immunity as a Mechanistic Bridge Between Uremic Toxins, Atherosclerosis, and Vascular Calcification in Chronic Kidney Disease.Cardiovascular toxicology · 2026Review
- OPA1 as a Cancer Target: Molecular Mechanisms, Structural Insights, and Strategies for Drug Development.Antioxidants (Basel, Switzerland) · 2026Review
- Cystinosis and Cellular Energy Failure: Mitochondria at the Crossroads.International journal of molecular sciences · 2026Review
- Modulation of mitochondrial quality control in sepsis by traditional Chinese medicine: mechanistic insights and translational perspectives.Frontiers in pharmacology · 2026Review
- Cyclophilin D reduces Ca2+ sequestration by complement 1q binding protein.The Biochemical journal · 2025Article
- Unveiling the protein landscape for early detection of colorectal precancerous lesions.Clinical proteomics · 2025Article
- C1QBP Modulates DNA Damage Response and Radiosensitivity in Hepatocellular Carcinoma by Regulating NF-κB Activity.International journal of molecular sciences · 2025Article
- Mitochondrial dynamics in cisplatin resistance: molecular mechanisms and therapeutic targeting.Frontiers in oncology · 2025Review
- Endogenous complement 1q binding protein (C1qbp) regulates mitochondrial permeability transition and post-myocardial infarction remodeling and dysfunction.Journal of molecular and cellular cardiology · 2024Article
- Aerobic Exercise Activates AMPK/PGC-1α Pathway, Inhibits Cardiomyocyte Apoptosis Improves Mitochondrial and Infarcted Heart Function.Doklady. Biochemistry and biophysics · 2024Article
- ROS Induced byMarine drugs · 2024Article
- QiDongNing induces lung cancer cell apoptosis via triggering P53/DRP1-mediated mitochondrial fission.Journal of cellular and molecular medicine · 2024Article
- Inhibition of Multifunctional Protein p32/C1QBP Promotes Cytostatic Effects in Colon Cancer Cells by Altering Mitogenic Signaling Pathways and Promoting Mitochondrial Damage.International journal of molecular sciences · 2024Article
- CHCHD2 up-regulation in Huntington disease mediates a compensatory protective response against oxidative stress.Cell death & disease · 2024Article
- p32/OPA1 axis-mediated mitochondrial dynamics contributes to cisplatin resistance in non-small cell lung cancer.Acta biochimica et biophysica Sinica · 2024Article
- p32 regulates glycometabolism and TCA cycle to inhibit ccRCC progression via copper-induced DLAT lipoylation oligomerization.International journal of biological sciences · 2024Article
- Mitochondria Deregulations in Cancer Offer Several Potential Targets of Therapeutic Interventions.International journal of molecular sciences · 2023Review
- C1QBP Mediates Breast Cancer Cell Proliferation and Growth via Multiple Potential Signalling Pathways.International journal of molecular sciences · 2023Article
- Aorta- and liver-generated TMAO enhances trained immunity for increased inflammation via ER stress/mitochondrial ROS/glycolysis pathways.JCI insight · 2023Article
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Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are dynamic organelles that undergo fusion and fission in response to various physiological and stress stimuli, which play key roles in diverse mitochondrial functions such as energy metabolism, intracellular signaling, and apoptosis. OPA1, a mitochondrial dynamin-like GTPase, is responsible for the inner membrane fusion of mitochondria, and the function of OPA1 is regulated by proteolytic cleavage in response to various metabolic stresses. Growing evidences highlighted the importance of mitochondrial adaptation in response to metabolic stimuli. Here, we demonstrated the role of p32/C1QBP in mitochondrial morphology by regulating OMA1-dependent proteolytic processing of OPA1. Genetic ablation of p32/C1QBP activates OMA1, cleaves OPA1, and leads mitochondrial fragmentation and swelling. The loss of p32/C1QBP decreased mitochondrial respiration and lipid utilization, sensitized cells to mitochondrial stress, and triggered a metabolic shift from oxidative phosphorylation to glycolysis, which were correlated with apoptosis in cancer cells and the inhibition of 3D-spheroid formation. These results suggest a unique regulation of cell physiology by mitochondria and provide a basis for a new therapeutic strategy for cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.