ArticleEMBO reports2021
Muscle-specific Cand2 is translationally upregulated by mTORC1 and promotes adverse cardiac remodeling.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 3 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 3 syntheses or guidelines pooled it, 22 citations in OpenAlex.
- Genome-wide analysis of heart failure yields insights into disease heterogeneity and enables prognostic prediction in the Japanese population.Nature communications · 2025Pooled it
- Genome-wide association study meta-analysis provides insights into the etiology of heart failure and its subtypes.Nature genetics · 2025Pooled it
- Using human induced pluripotent stem cell-derived cardiomyocytes to understand the mechanisms driving cardiomyocyte maturation.Frontiers in cardiovascular medicine · 2022Pooled it
- Development of a protein synthesis network at the sarco/endoplasmic reticulum in adult cardiac myocytes.The Journal of physiology · 2026Article
- CAND1 and CAND2 drive CUL4 substrate receptor exchange with largely comparable biochemical efficiency, unlike their relative effects on CUL1.Structure (London, England : 1993) · 2026Article
- RMC-6272, a selective third-generation bi-steric mTORC1 inhibitor, improves cardiac function in pressure overload-induced cardiac hypertrophy.Journal of molecular and cellular cardiology plus · 2026Article
- Molecular mechanisms of CAND2 in regulating SCF ubiquitin ligases.Nature communications · 2025Article
- Genome-wide association study reveals mechanisms underlying dilated cardiomyopathy and myocardial resilience.Nature genetics · 2024Article
- Transient Inhibition of Translation Improves Cardiac Function After Ischemia/Reperfusion by Attenuating the Inflammatory Response.Circulation · 2024Article
- Spatial Transcriptomic Profiling of Human Saphenous Vein Exposed to Ex Vivo Arterial Haemodynamics-Implications for Coronary Artery Bypass Graft Patency and Vein Graft Disease.International journal of molecular sciences · 2024Article
- Whole Exome Sequencing of Thymoma Patients Exhibiting Exceptional Responses to Pemetrexed Monotherapy.Cancers · 2023Article
- mTORC1 inhibition impairs activation of the unfolded protein response and induces cell death during ER stress in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2023Article
- Translational control of Ybx1 expression regulates cardiac function in response to pressure overload in vivo.Basic research in cardiology · 2023Article
- Roles of Cullin-RING Ubiquitin Ligases in Cardiovascular Diseases.Biomolecules · 2022Review
- Integration of RNA-seq and ATAC-seq identifies muscle-regulated hub genes in cattle.Frontiers in veterinary science · 2022Article
- Muscle-specific Cand2 is translationally upregulated by mTORC1 and promotes adverse cardiac remodeling.EMBO reports · 2021Article
Corrections and comments
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanistic target of rapamycin (mTOR) promotes pathological remodeling in the heart by activating ribosomal biogenesis and mRNA translation. Inhibition of mTOR in cardiomyocytes is protective; however, a detailed role of mTOR in translational regulation of specific mRNA networks in the diseased heart is unknown. We performed cardiomyocyte genome-wide sequencing to define mTOR-dependent gene expression control at the level of mRNA translation. We identify the muscle-specific protein Cullin-associated NEDD8-dissociated protein 2 (Cand2) as a translationally upregulated gene, dependent on the activity of mTOR. Deletion of Cand2 protects the myocardium against pathological remodeling. Mechanistically, we show that Cand2 links mTOR signaling to pathological cell growth by increasing Grk5 protein expression. Our data suggest that cell-type-specific targeting of mTOR might have therapeutic value against pathological cardiac remodeling.
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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.