ArticlePloS one2013
Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Role of CR6-Interacting Factor 1 (Crif1) in Cardiac Mitochondrial Structure and Stress-Induced Functional Decline.Korean circulation journal · 2026Article
- SIRT1: The first key to unlocking the mystery of cardiovascular diseases.Frontiers in pharmacology · 2025Review
- Article
- Beneficial Effects of Low-Grade Mitochondrial Stress on Metabolic Diseases and Aging.Yonsei medical journal · 2024Review
- Mitochondrial Cardiomyopathy: Molecular Epidemiology, Diagnosis, Models, and Therapeutic Management.Cells · 2022Review
- SIRT1 Activation Attenuates the Cardiac Dysfunction Induced by Endothelial Cell-Specific Deletion of CRIF1.Biomedicines · 2021Article
- Deficiency of Crif1 in hair follicle stem cells retards hair growth cycle in adult mice.PloS one · 2020Article
- Targeted deletion of Crif1 in mouse epidermis impairs skin homeostasis and hair morphogenesis.Scientific reports · 2017Article
- Co-Activation of PKC-δ by CRIF1 Modulates Oxidative Stress in Bone Marrow Multipotent Mesenchymal Stromal Cells after Irradiation by Phosphorylating NRF2 Ser40.Theranostics · 2017Article
- Article
- Lymphocyte-specific protein tyrosine kinase (Lck) interacts with CR6-interacting factor 1 (CRIF1) in mitochondria to repress oxidative phosphorylation.BMC cancer · 2015Article
- Disruption of CR6-interacting factor-1 (CRIF1) in mouse islet beta cells leads to mitochondrial diabetes with progressive beta cell failure.Diabetologia · 2015Article
- Role of Energy Metabolism in the Brown Fat Gene Program.Frontiers in endocrinology · 2015Review
- Mechanism of androgen receptor corepression by CKβBP2/CRIF1, a multifunctional transcription factor coregulator expressed in prostate cancer.Molecular and cellular endocrinology · 2014Article
- The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are key organelles dedicated to energy production. Crif1, which interacts with the large subunit of the mitochondrial ribosome, is indispensable for the mitochondrial translation and membrane insertion of respiratory subunits. To explore the physiological function of Crif1 in the heart, Crif1(f/f) mice were crossed with Myh6-cre/Esr1 transgenic mice, which harbor cardiomyocyte-specific Cre activity in a tamoxifen-dependent manner. The tamoxifen injections were given at six weeks postnatal, and the mutant mice survived only five months due to hypertrophic heart failure. In the mutant cardiac muscles, mitochondrial mass dramatically increased, while the inner structure was altered with lack of cristae. Mutant cardiac muscles showed decreased rates of oxygen consumption and ATP production, suggesting that Crif1 plays a critical role in the maintenance of both mitochondrial structure and respiration in cardiac muscles.
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Registered trials
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.