ArticleMolecular medicine (Cambridge, Mass.)2023
Aerobic exercise improves cognitive impairment in mice with type 2 diabetes by regulating the MALAT1/miR-382-3p/BDNF signaling pathway in serum-exosomes.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 4 of them syntheses that pooled it.
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Who cites it
27 citing papers in PubMed, 4 syntheses or guidelines pooled it, 32 citations in OpenAlex.
- The effect of different exercise interventions on global cognitive function in patients with type 2 diabetes: a systematic review and network meta-analysis.BMC public health · 2026Pooled it
- Effect of exercise on brain-derived neurotrophic factors in middle-aged and older adults with type 2 diabetes mellitus: a systematic review and meta-analysis.Frontiers in physiology · 2025Pooled it
- Meta-analysis of the effect of exercise intervention on cognitive function in elderly patients with type 2 diabetes mellitus.BMC geriatrics · 2024Pooled it
- The Effect of Physical Activity/Exercise on miRNA Expression and Function in Non-Communicable Diseases-A Systematic Review.International journal of molecular sciences · 2024Pooled it
- Exercise-Induced Regulation of LncRNAs: Mechanistic Insights and Clinical Translation in Cardiovascular Health.Journal of cardiovascular translational research · 2026Review
- Harnessing exosomal long non-coding RNAs as a new frontier for molecular diagnostics and therapeutics in diabetes mellitus.Cell communication and signaling : CCS · 2026Review
- The Jekyll and Hyde of Extracellular Vesicles: Dual Roles as Disease Drivers and Therapeutic Saviors in Diabetic Brain.Molecular neurobiology · 2026Review
- Exosomal MicroRNAs as theranostic tools in type 2 diabetes and its complications: mechanistic insights and clinical implications.Diabetology & metabolic syndrome · 2026Review
- Exercise-derived exosomes: molecular mediators of systemic health and disease therapy.Journal of nanobiotechnology · 2026Review
- Research Progress on Pathology, Molecular Mechanisms, and Intervention Strategies of Cognitive Dysfunction Associated with Type 2 Diabetes.International journal of general medicine · 2026Review
- Exercise-conditioned extracellular vesicles in Alzheimer's disease: a multi-organ signaling network linking peripheral adaptation to brain pathology.Frontiers in immunology · 2026Review
- Exosomes: emerging biomarkers and therapeutic potential in postoperative delirium and postoperative cognitive dysfunction.Frontiers in cell and developmental biology · 2026Review
- The diabetic retina-brain axis hypothesis in diabetic cognitive impairment: from pathophysiological mechanisms to therapeutic implications.Frontiers in endocrinology · 2026Review
- Crosstalk between skeletal muscle and the brain during physical activity - in search of epigenetic mechanisms.Epigenetics · 2025Review
- Long Non-Coding RNAs in Diabetic Cardiomyopathy: Potential Function as Biomarkers and Therapeutic Targets of Exercise Training.Journal of cardiovascular translational research · 2025Review
- Expert consensus statement for basic research of animal exercise intervention studies in chronic disease prevention and treatment: A joint position paper of the Exercise Science branch of the Biophysical Society of China and the Metabolism and Genetics branch of the Genetics Society of China.Journal of sport and health science · 2025Article
- Investigating the Therapeutic Mechanisms of Shen-Ling-Bai-Zhu-San in Type 2 Diabetes and Ulcerative Colitis Comorbidity: A Network Pharmacology and Molecular Simulation Approach.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The impact of ncRNAs on type 2 diabetes: A comprehensive review covering molecular mechanisms to clinical applications.Molecular therapy. Nucleic acids · 2025Review
- Effects of aerobic and anaerobic exercise on glucose, lipid, and inflammation-related gene expression in the brain tissue of streptozotocin-induced diabetic rat model.Diabetology & metabolic syndrome · 2025Article
- Risk Factors, Pathological Changes, and Potential Treatment of Diabetes-Associated Cognitive Dysfunction.Journal of diabetes · 2025Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt has been documented that aerobic exercise (AE) has a positive effect on improving cognitive function in type 2 diabetes (T2DM) patients. Here, we tried to explore how AE regulates the expression of long non-coding RNA in serum-exosomes (Exos), thereby affecting cognitive impairment in T2DM mice as well as its potential molecular mechanism.
methodsT2DM mouse models were constructed, and serum-Exos were isolated for whole transcriptome sequencing to screen differentially expressed lncRNA and mRNA, followed by prediction of downstream target genes. The binding ability of miR-382-3p with a long non-coding RNA MALAT1 and brain-derived neurotrophic factor (BDNF) was explored. Then, primary mouse hippocampal neurons were collected for in vitro mechanism verification, as evidenced by the detection of hippocampal neurons' vitality, proliferation, and apoptosis capabilities, and insulin resistance. Finally, in vivo mechanism verification was performed to assess the effect of AE on insulin resistance and cognitive disorder.
resultsTranscriptome sequencing analysis showed that MALAT1 was lowly expressed and miR-382-3p was highly expressed in serum-Exos samples of T2DM mice. There were targeted binding sites between MALAT1 and miR-382-3p and between miR-382-3p and BDNF. In vitro experiments showed that MALAT1 upregulated BDNF expression by inhibiting miR-382-3p. Silencing MALAT1 or overexpressing miR-382-3p could reduce the expression of INSR, IRS-1, IRS-2, PI3K/AKT, and Ras/MAPK, inhibit neuronal proliferation, and promote apoptosis. In vivo experiments further confirmed that AE could increase the expression of MALAT1 in serum-Exos to competitively inhibit miR-382-3p and upregulate BDNF expression, thereby improving cognitive impairment in T2DM mice.
conclusionAE may upregulate the expression of MALAT1 in serum-Exos to competitively inhibit miR-382-3p and upregulate BDNF expression, thus improving cognitive impairment in T2DM mice.
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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 Socratic graph.