ArticleCell reports2018
Cardiac mTORC1 Dysregulation Impacts Stress Adaptation and Survival in Huntington's Disease.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Application of Neurotrophic Factors as a Therapeutic Approach for Neurodegenerative Diseases.Experimental neurobiology · 2025Review
- Atrial fibrillation risk model based on LASSO and SVM algorithms and immune infiltration of key mitochondrial energy metabolism genes.Scientific reports · 2025Article
- Santalum album L. alleviates cardiac function injury in heart failure by synergistically inhibiting inflammation, oxidative stress and apoptosis through multiple components.Chinese medicine · 2024Article
- Metabolism in Huntington's disease: a major contributor to pathology.Metabolic brain disease · 2022Review
- Huntington's disease phenotypes are improved via mTORC1 modulation by small molecule therapy.PloS one · 2022Article
- Systemic manifestation and contribution of peripheral tissues to Huntington's disease pathogenesis.Ageing research reviews · 2021Review
- Purine Nucleotides Metabolism and Signaling in Huntington's Disease: Search for a Target for Novel Therapies.International journal of molecular sciences · 2021Review
- Effects of mutant huntingtin inactivation on Huntington disease-related behaviours in the BACHD mouse model.Neuropathology and applied neurobiology · 2021Article
- MicroRNAs Regulating Autophagy in Neurodegeneration.Advances in experimental medicine and biology · 2021Article
- Progressive cardiac arrhythmias and ECG abnormalities in the Huntington's disease BACHD mouse model.Human molecular genetics · 2020Article
- Modeling Polyglutamine Expansion Diseases with Induced Pluripotent Stem Cells.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Mammalian Target of Rapamycin: A Metabolic Rheostat for Regulating Adipose Tissue Function and Cardiovascular Health.The American journal of pathology · 2019Review
- Drp1/Fis1-mediated mitochondrial fragmentation leads to lysosomal dysfunction in cardiac models of Huntington's disease.Journal of molecular and cellular cardiology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Huntington's disease (HD) is a dominantly inherited neurological disorder caused by CAG-repeat expansion in exon 1 of Huntingtin (HTT). But in addition to the neurological disease, mutant HTT (mHTT), which is ubiquitously expressed, impairs other organ systems. Indeed, epidemiological and animal model studies suggest higher incidence of and mortality from heart disease in HD. Here, we show that the protein complex mTORC1 is dysregulated in two HD mouse models through a mechanism that requires intrinsic mHTT expression. Moreover, restoring cardiac mTORC1 activity with constitutively active Rheb prevents mortality and relieves the mHTT-induced block to hypertrophic adaptation to cardiac stress. Finally, we show that chronic mTORC1 dysregulation is due in part to mislocalization of endogenous Rheb. These data provide insight into the increased cardiac-related mortality of HD patients, with cardiac mHTT expression inhibiting mTORC1 activity, limiting heart growth, and decreasing the heart's ability to compensate to chronic stress.
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