ArticleBMC biology2017
MicroRNA miR-29 controls a compensatory response to limit neuronal iron accumulation during adult life and aging.
Article in BMC biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- What role do extracellular vesicles play in developing physical frailty and sarcopenia? : A systematic review.Zeitschrift fur Gerontologie und Geriatrie · 2023Pooled it
- MicroRNA-29 acutely regulates memory stability, expression of synaptic genes, and DNA methylation in the mouse adult hippocampus.Cellular and molecular life sciences : CMLS · 2026Article
- Genetic and Environmental Factors Shaping Hearing Loss: Xenobiotics, Mechanisms and Translational Perspectives.Journal of xenobiotics · 2026Review
- Role of Compensatory miRNA Networks in Cognitive Recovery from Heart Failure.Non-coding RNA · 2025Article
- Insights into targeted ferroptosis in mechanisms, biology, and role of Alzheimer's disease: an update.Frontiers in aging neuroscience · 2025Review
- Regulating translation in aging: from global to gene-specific mechanisms.EMBO reports · 2024Review
- The role of MicroRNAs as fine-tuners in the onset of puberty: a comprehensive review.Annals of pediatric endocrinology & metabolism · 2024Article
- Human Aging and Age-Related Diseases: From Underlying Mechanisms to Pro-Longevity Interventions.Aging and disease · 2024Review
- Plasma miRNAs as potential biomarkers for schizophrenia in a Jordanian cohort.Non-coding RNA research · 2024Article
- 12-HETE activates Müller glial cells: The potential role of GPR31 and miR-29.Prostaglandins & other lipid mediators · 2024Article
- MicroRNA biomarkers as next-generation diagnostic tools for neurodegenerative diseases: a comprehensive review.Frontiers in molecular neuroscience · 2024Review
- Nuclear miR-150 enhances hepatic lipid accumulation by targeting RNA transcripts overlapping theiScience · 2023Article
- Up-regulated expression of miRNA-29b in patients with Parkinson's disease on levodopa gel infusion.Acta neurologica Belgica · 2023Article
- Exploring Whether Iron Sequestration within the CNS of Patients with Alzheimer's Disease Causes a Functional Iron Deficiency That Advances Neurodegeneration.Brain sciences · 2023Article
- Review
- Role of noncoding RNAs in cardiac ageing.Frontiers in cardiovascular medicine · 2023Review
- Review
- Editorial for Special Issue: "MicroRNA in Cardiac Health and Disease".International journal of molecular sciences · 2022Article
- Adaptive cellular response of the substantia nigra dopaminergic neurons upon age-dependent iron accumulation.Aging cell · 2022Article
- MircoRNA-29a in Astrocyte-derived Extracellular Vesicles Suppresses Brain Ischemia Reperfusion Injury via TP53INP1 and the NF-κB/NLRP3 Axis.Cellular and molecular neurobiology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA widespread modulation of gene expression occurs in the aging brain, but little is known as to the upstream drivers of these changes. MicroRNAs emerged as fine regulators of gene expression in many biological contexts and they are modulated by age. MicroRNAs may therefore be part of the upstream drivers of the global gene expression modulation correlated with aging and aging-related phenotypes.
resultsHere, we show that microRNA-29 (miR-29) is induced during aging in short-lived turquoise killifish brain and genetic antagonism of its function induces a gene-expression signature typical of aging. Mechanicistically, we identified Ireb2 (a master gene for intracellular iron delivery that encodes for IRP2 protein), as a novel miR-29 target. MiR-29 is induced by iron loading and, in turn, it reduces IRP2 expression in vivo, therefore limiting intracellular iron delivery in neurons. Genetically modified fish with neuro-specific miR-29 deficiency exhibit increased levels of IRP2 and transferrin receptor, increased iron content, and oxidative stress.
conclusionsOur results demonstrate that age-dependent miR-29 upregulation is an adaptive mechanism that counteracts the expression of some aging-related phenotypes and its anti-aging activity is primarily exerted by regulating intracellular iron homeostasis limiting excessive iron-exposure in neurons.
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Registered trials
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