ArticleNature medicine2013
Tsc1 (hamartin) confers neuroprotection against ischemia by inducing autophagy.
Article in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
129 citing papers in PubMed, 232 citations in OpenAlex.
- Trial
- An integrated investigation of systemic and localized pathophysiological mechanisms of stroke and multimodal therapeutic strategies.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Neurochemical Mechanisms Underlying Tanshinone-Mediated Neuroprotection and Formulation Strategies in Cerebral Ischemia/Reperfusion Injury.Neurochemical research · 2026Review
- Article
- No-reflow phenomenon after vessel recanalization in acute ischemic stroke: mechanisms, diagnosis, and treatment directions.Journal of neurology · 2026Review
- Unveiling the neuroprotective power: the role of autophagy in remote ischemic conditioning.Metabolic brain disease · 2025Review
- Sex-Dependent Regional Vulnerability and Recovery Mechanisms in a Mouse Model of Transient Global Cerebral Ischemia.Neuromolecular medicine · 2025Article
- Epilepsy and autophagy modulators: a therapeutic split.Autophagy · 2025Review
- Upregulating mTOR/S6 K Pathway by CASTOR1 Promotes Astrocyte Proliferation and Myelination in GpamMolecular neurobiology · 2025Article
- Rapamycin Treatment Reduces Brain Pericyte Constriction in Ischemic Stroke.Translational stroke research · 2025Article
- Traumatic Brain Injury and Alzheimer's Disease: A Shared Neurovascular Hypothesis.Neuroscience insights · 2025Review
- Astragaloside IV improves the survival rates of retinal ganglion cells in traumatic optic neuropathy by regulating autophagy mediated by the AMPK-MTOR-ULK signaling pathway.Molecular vision · 2025Article
- Ischemic Stroke and the Biological Hallmarks of Aging.Aging and disease · 2024Review
- Activation of SIRT1/Nrf2/HO-1 and Beclin-1/AMPK/mTOR autophagy pathways by eprosartan ameliorates testicular dysfunction induced by testicular torsion in rats.Scientific reports · 2024Article
- Astrocyte-Derived Extracellular Vesicles for Ischemic Stroke: Therapeutic Potential and Prospective.Aging and disease · 2024Review
- The Multiple Roles of Autophagy in Neural Function and Diseases.Neuroscience bulletin · 2024Review
- Shared Proteins and Pathways of Cardiovascular and Cognitive Diseases: Relation to Vascular Cognitive Impairment.Journal of proteome research · 2024Article
- The neuroprotective effect of Chinese herbal medicine for cerebral ischemia reperfusion injury through regulating mitophagy.Frontiers in pharmacology · 2024Review
- Role of autophagy in ischemic stroke: insights from animal models and preliminary evidence in the human disease.Frontiers in cell and developmental biology · 2024Review
- Reinventing the Penumbra - the Emerging Clockwork of a Multi-modal Mechanistic Paradigm.Translational stroke research · 2023Review
69 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
Abstract
Previous attempts to identify neuroprotective targets by studying the ischemic cascade and devising ways to suppress it have failed to translate to efficacious therapies for acute ischemic stroke. We hypothesized that studying the molecular determinants of endogenous neuroprotection in two well-established paradigms, the resistance of CA3 hippocampal neurons to global ischemia and the tolerance conferred by ischemic preconditioning (IPC), would reveal new neuroprotective targets. We found that the product of the tuberous sclerosis complex 1 gene (TSC1), hamartin, is selectively induced by ischemia in hippocampal CA3 neurons. In CA1 neurons, hamartin was unaffected by ischemia but was upregulated by IPC preceding ischemia, which protects the otherwise vulnerable CA1 cells. Suppression of hamartin expression with TSC1 shRNA viral vectors both in vitro and in vivo increased the vulnerability of neurons to cell death following oxygen glucose deprivation (OGD) and ischemia. In vivo, suppression of TSC1 expression increased locomotor activity and decreased habituation in a hippocampal-dependent task. Overexpression of hamartin increased resistance to OGD by inducing productive autophagy through an mTORC1-dependent mechanism.
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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.