Nur77 Mediates Anaphylaxis by Regulating miR-21a.
Jo H, Jeoung J, Shim K, Jeoung D
This study identifies Nur77 as a key driver of allergic reactions, specifically anaphylaxis, by regulating miR-21a and inflammatory markers in mast cells. The findings suggest that targeting the Nur77-miR-21a pathway could lead to new anti-allergy treatments.
- Nur77 promotes allergic inflammation and anaphylaxis symptoms in cell and animal models.
- Blocking Nur77 reduces inflammatory markers like COX2 and MCP1 in mast cells.
- miR-21a acts as a negative regulator of Nur77, suppressing allergic responses.
- The study proposes the Nur77-miR-21a loop as a target for anti-allergy drugs.
Melatonin promotes cell cycle progression of neural stem cells subjected to manganese via Nurr1.
Chen N, Zhou H, He B, Peng S, Ding F, Liu QH, Ma Z, Liu W, Xu B
Melatonin protects neural stem cells from manganese-induced damage by activating Nurr1 to restore normal cell division. This mechanism suggests that melatonin could potentially counteract environmental toxins that disrupt brain development.
- Manganese exposure arrests neural stem cell growth by disrupting key cell cycle proteins.
- Melatonin reverses this arrest and restores cell proliferation in neural stem cells.
- The protective effect of melatonin depends entirely on the presence of Nurr1.
- Blocking Nurr1 eliminates melatonin's ability to protect cells from manganese toxicity.
Zona Glomerulosa-Derived Klotho Modulates Aldosterone Synthase Expression in Young Female Mice.
Daryadel A, Tang C, Xie Y, Peitzsch M, Fisi V, Hantel C, Loffing-Cueni D, Breault DT, Penton D, Loffing J, Beuschlein F
Klotho produced in the adrenal zona glomerulosa helps regulate the gene that makes aldosterone, but reducing it in young female mice doesn't change aldosterone levels or blood pressure. Instead, the gene for aldosterone production and its regulators become more active, suggesting a complex internal control system.
- Zona glomerulosa Klotho regulates aldosterone-making genes
- Lower Klotho didn’t raise aldosterone or blood pressure in young mice
- The aldosterone gene and its activators increased despite less Klotho
- Klotho’s role may change with age or diet
- Findings suggest internal adrenal regulation, not systemic effects
A Graphene Composite Film Based Wearable Far-Infrared Therapy Apparatus (GRAFT) for Effective Prevention of Postoperative Peritoneal Adhesion.
Lu X, Xu L, Song Y, Yu X, Li Q, Liu F, Li X, Xi J, Wang S, Wang L, Wang Z
This study developed a wearable device using graphene film to emit far-infrared light that reduces post-surgical abdominal adhesions in animals by calming harmful inflammation through immune cells. The treatment works by boosting a gene called NR4A2, which helps switch immune cells to a healing state, significantly lowering adhesion formation. The device showed strong results in both rats and pigs, with no skin damage and better outcomes than current treatments.
- Far-infrared light reduces abdominal adhesions in animals
- The treatment boosts NR4A2 to calm harmful immune responses
- A wearable device (GRAFT) delivers therapy without skin damage
- Results outperformed current clinical treatments in animal models
- NR4A2 activation helps switch immune cells to healing mode
Relapse to cocaine seeking is regulated by medial habenula NR4A2/NURR1 in mice.
Childs JE, Morabito S, Das S, Santelli C, Pham V, Kusche K, Vera VA, Reese F, Campbell RR, Matheos DP, Swarup V, Wood MA
This study shows that NR4A2 in a specific mouse brain region controls relapse to drug-seeking behavior, but it provides no information about human development or treatment for NR4A2-related syndromes. The findings are limited to molecular mechanisms in mice and do not translate to clinical insights for children with this genetic condition.
- Research uses mice, not humans, limiting direct applicability to pediatric care.
- Focuses on cocaine relapse, which is unrelated to NR4A2 syndrome symptoms.
- Identifies NR4A2's role in addiction circuits, not developmental biology.
- No evidence for treatment strategies or phenotypic management in humans.
Vascular Endothelial Cell-Derived Exosomal Sphingosylphosphorylcholine Attenuates Myocardial Ischemia-Reperfusion Injury through NR4A2-Mediated Mitophagy.
Yu Y, Li Z, Cai Y, Guo J, Lin Y, Zhao J
This study shows that a specific lipid molecule delivered by cell vesicles protects heart muscle from damage caused by lack of blood flow. The protection works by activating a cellular cleanup process called mitophagy, which relies on the NR4A2 protein. This research focuses entirely on heart disease mechanisms in mice and cells.
- VEC-derived exosomes carrying SPC reduce heart damage in mouse models of ischemia-reperfusion injury.
- SPC activates the NR4A2/OPTN pathway to increase mitophagy in cardiomyocytes.
- Increased mitophagy prevents apoptosis and improves survival of heart muscle cells after injury.
- The findings suggest SPC-rich exosomes could be therapeutic targets for myocardial infarction.
Investigating the Effect of an Anti-Inflammatory Drug in Determining NURR1 Expression and Thus Exploring the Progression of Parkinson's Disease.
Zheng X, Zhao Z, Zhao L
Ibuprofen restores motor function and increases NURR1 expression in mice with early-stage Parkinson's disease but fails to help those with advanced disease. This suggests that the timing of anti-inflammatory intervention is critical for affecting NURR1 levels and neuroprotection in this model.
- Ibuprofen improves motor skills and NURR1 levels only in early-stage Parkinson's mice.
- Advanced Parkinson's mice show no benefit from ibuprofen treatment regarding function or NURR1.
- NURR1 appears to mediate the anti-inflammatory and neuroprotective effects of ibuprofen.
- The study uses an MPTP-induced mouse model, not human patients.
Metabolomic modelling and neuroprotective effects of carvacrol against acrylamide toxicity in rat's brain and sciatic nerve.
Durmus H, Burak AM, Goktug S, Aysegul B
Acrylamide harms the brain and nerves, but carvacrol reduces this damage by boosting antioxidant defenses and restoring levels of the NR4A2 protein, which is important for nerve health. This study shows carvacrol protects both central and peripheral nerves in rats exposed to acrylamide.
- Acrylamide damages brain and nerve tissue
- Carvacrol boosts protective antioxidants
- Carvacrol restores NR4A2 levels
- Carvacrol reduces nerve inflammation and degeneration
- Findings suggest carvacrol may help protect nerves
Promoting collateral formation in type 2 diabetes mellitus using ultra-small nanodots with autophagy activation and ROS scavenging.
Wang Y, Li F, Mao L, Liu Y, Chen S, Liu J, Huang K, Chen Q, Wu J, Lu L, Zheng Y, Shen W, Ying T, Dai Y, Shen Y
This study demonstrates that molybdenum disulfide nanodots improve blood vessel formation in diabetic mice by activating autophagy through the NR4A2 pathway. The findings rely entirely on animal models and cell cultures, with no evidence of human application or clinical relevance to NR4A2-related neurodevelopmental syndromes.
- The research focuses on type 2 diabetes and cardiovascular disease, not neurological development.
- NR4A2 is studied only as a molecular mechanism for vascular repair in diabetic models.
- No human data, patient cohorts, or clinical trials are included in this work.
- The therapeutic agent is a synthetic nanodot with no direct link to NR4A2 genetics.
Orphan Nuclear Receptor Family 4A (NR4A) Members NR4A2 and NR4A3 Selectively Modulate Elements of the Monocyte Response to Buffered Hypercapnia.
Phelan DE, Reddan B, Shigemura M, Sznajder JI, Crean D, Cummins EP
NR4A2 and NR4A3 are transcription factors that help regulate how monocytes respond to high carbon dioxide levels, a condition linked to lung diseases. Depleting these proteins reduces the cells' ability to adjust key genes involved in energy production and stress response, but other factors also play a role.
- NR4A2 and NR4A3 respond to high CO2 in immune cells
- These proteins control stress and energy-related genes in monocytes
- Other factors besides NR4A2/3 also influence the CO2 response
- New candidate genes like ETS-1 may be involved in CO2 sensing
Preconditioning exercise reduces brain damage of ischemic stroke in rats via PI3K-AKT pathway by bioinformatic analysis.
Li K, Gao ZK, Guo YS, Shen XY, Han Y, Yuan M, Bi X
Preconditioning exercise reduces brain damage and improves neurological function in rats after ischemic stroke by regulating the PI3K-AKT pathway. The study identifies NR4A2 as one of several key genes involved in this protective mechanism, alongside Foxd3, Foxa2, SP1, CEBPA, and SOX10.
- Exercise preconditioning reduces infarct size and apoptosis in rat stroke models.
- Protection occurs via the PI3K-AKT pathway promoting angiogenesis.
- NR4A2 interacts with other key genes in this protective network.
- This is a preclinical animal study, not human clinical evidence.
The nuclear receptor Nurr1 is preferentially expressed in human pro-inflammatory macrophages and limits their inflammatory profile.
Solís-Barbosa MA, Santana E, Muñoz-Torres JR, Segovia-Gamboa NC, Patiño-Martínez E, Meraz-Ríos MA, Samaniego R, Sánchez-Mateos P, Sánchez-Torres C
Nurr1 acts as a brake on inflammation in human macrophages by reducing the production of key inflammatory signals. This regulatory mechanism involves Nurr1 interacting with NF-κB to limit its activity, suggesting a potential pathway for controlling excessive immune responses.
- Nurr1 is highly expressed in pro-inflammatory human macrophages.
- Activating Nurr1 reduces the release of multiple inflammatory cytokines.
- Nurr1 limits inflammation by inhibiting NF-κB transcriptional activity.
- This study focuses on general immune cell regulation, not NR4A2 syndrome.
[Rho kinase inhibitor Y27632 promotes survival of human induced pluripotent stem cells during differentiation into functional midbrain dopaminergic progenitor cells in vitro].
Li Y, Xu J, Jiang C, Chen Z, Chen Y, Ying M, Wang A, Ma C, Wang C, Guo Y, Liu C
Adding the drug Y27632 to human stem cell cultures improves the survival of cells as they begin to develop into dopamine-producing neurons. This increased survival rate leads to a higher overall yield of these specific neural progenitor cells in laboratory settings.
- Y27632 boosts cell survival during early differentiation into midbrain dopaminergic progenitors.
- The drug reduces apoptosis without interfering with the final neuronal identity.
- This is an in vitro study using human induced pluripotent stem cells.
- No clinical trials or human patient data are included.
The Synergistic Effect Study of Lipopolysaccharide (LPS) and A53T-α-Synuclein: Intranasal LPS Exposure on the A53T-α-Synuclein Transgenic Mouse Model of Parkinson's Disease.
He Q, Zhang S, Wang J, Ma T, Ma D, Wu L, Zhou M, Zhao L, Chen Y, Liu J, Chen W
Intranasal exposure to bacterial toxins accelerates Parkinson's-like symptoms in mice carrying a specific alpha-synuclein mutation. This process involves inflammation that suppresses Nurr1, a protein critical for dopamine neuron survival, leading to increased neuronal loss and motor deficits. The study highlights how environmental triggers can worsen genetic risks through inflammatory pathways.
- Intranasal LPS worsens symptoms in alpha-synuclein mutant mice.
- Bacterial toxins trigger brain inflammation that suppresses Nurr1.
- Nurr1 inhibition leads to dopamine neuron loss and motor issues.
- Aging amplifies the negative effects of genetic and environmental factors.
A simple and reliable method for claustrum localization across age in mice.
Shaker T, Dagpa GJ, Cattaud V, Marriott BA, Sultan M, Almokdad M, Jackson J
This study developed a reliable method to identify claustrum neurons in mice using a combination of Nurr1 and Tle4 markers, which helps distinguish claustrum cells from nearby cortical cells, especially during early development when other methods fail. The technique works across ages and confirms that claustrum neurons activate in response to novelty, supporting their role in sensory integration.
- Uses Nurr1 and Tle4 to clearly identify claustrum neurons
- Works in newborn mice when other methods fail
- Confirms claustrum activation during novelty exposure
- Improves accuracy in developmental and functional studies
Oxidized low-density lipoproteins impair the pro-atherosclerotic effect of granulocyte-macrophage-colony-stimulating factor-producing T helper cells on macrophages.
Xiong X, Yan Z, Yan L, Yang X, Li D, Lin G
Oxidized lipids suppress immune cells that drive inflammation in blood vessels by activating NR4A2, which blocks their ability to stimulate macrophages. This mechanism is specific to vascular biology and atherosclerosis, with no established link to the neurodevelopmental or dopaminergic symptoms seen in NR4A2-related syndromes.
- NR4A2 activation by oxidized lipids inhibits T-helper cells in blood vessels.
- This reduces inflammation and foam cell formation in atherosclerosis models.
- The study focuses on vascular disease, not brain development or dopamine.
- No clinical data or relevance to NR4A2 neurodevelopmental phenotypes is presented.
Parallel expression patterns of NR4A nuclear receptor family genes in the pituitary gland of proestrus rats.
Terashima R, Nagao D, Ikeo M, Morioka K, Laoharatchatathanin T, Kurusu S, Kawaminami M
NR4A1, NR4A2, and NR4A3 genes are all activated together in the rat pituitary during the proestrus phase, which coincides with hormone surges before ovulation. This suggests these genes work in concert to regulate pituitary hormone production, particularly prolactin and luteinizing hormone.
- NR4A1, NR4A2, and NR4A3 rise together in the pituitary during proestrus
- Their activation matches hormone surges linked to ovulation
- NR4A2 is found in cells that produce reproductive hormones
- Estrogen and hormone signals boost NR4A gene expression
- NR4A genes may help control pituitary function before ovulation
Precision medicine for psychotic disorders: objective assessment, risk prediction, and pharmacogenomics.
Hill MD, Gill SS, Le-Niculescu H, MacKie O, Bhagar R, Roseberry K, Murray OK, Dainton HD, Wolf SK, Shekhar A, Kurian SM, Niculescu AB
This study identifies NR4A2 as one of several blood-based gene expression biomarkers associated with delusions in psychotic disorders. The research focuses on using these markers to predict psychiatric hospitalizations and guide medication choices for schizophrenia, rather than investigating NR4A2's role in developmental syndromes.
- NR4A2 appears in a blood gene signature linked to delusions in psychosis.
- The study targets schizophrenia treatment via pharmacogenomics, not developmental disorders.
- No clinical data or relevance for NR4A2-related syndrome is provided.
- Biomarkers suggest existing drugs like clozapine may help specific patient subgroups.
Structural characterization of the DNA binding mechanism of retinoic acid-related orphan receptor gamma.
Jiang L, Liu X, Liang X, Dai S, Wei H, Guo M, Chen Z, Xiao D, Chen Y
This study determines the atomic structure of how a different nuclear receptor, RORγ, binds to DNA as a dimer. It contrasts this with NR4A2, showing that NR4A2 binds to the same DNA sequence as a monomer instead.
- RORγ binds DNA as a homodimer using its C-terminal extension for recognition.
- NR4A2 binds the identical DR2 DNA site as a monomer, not a dimer.
- The structure reveals specific atomic interactions between RORγ and DNA.
- This is basic molecular biology with no clinical or therapeutic implications.
Pathological features and molecular signatures of early olfactory dysfunction in 3xTg-AD model mice.
Yu H, Wang F, Jia D, Bi S, Gong J, Wu JJ, Mao Y, Chen J, Chai GS
This study identifies reduced levels of the NR4A2 protein in the olfactory bulbs of mice with Alzheimer's disease, linking this drop to early smell loss. The findings suggest that NR4A2 plays a role in maintaining neuronal activity and could be a target for treating sensory deficits in neurodegenerative conditions.
- NR4A2 protein levels decrease in the olfactory bulbs of Alzheimer's model mice.
- This reduction correlates with early olfactory dysfunction before memory loss appears.
- The study focuses on Alzheimer's pathology, not NR4A2-related developmental syndromes.
- No human data or clinical trials involving NR4A2 are presented.
Nr4a2 blocks oAβ-mediated synaptic plasticity dysfunction and ameliorates spatial memory deficits in the APP Sw,Ind mouse.
Català-Solsona J, Lutzu S, Lituma PJ, Fábregas-Ordoñez C, Siedlecki D, Giménez-Llort L, Miñano-Molina AJ, Saura CA, Castillo PE, Rodriguez-Álvarez J
This study shows that activating the Nr4a2 protein can prevent synaptic damage and improve memory in mice with Alzheimer's-like symptoms. It identifies a mechanism where amyloid-beta blocks Nr4a2, suggesting that boosting Nr4a2 activity might protect brain cells from this specific type of damage.
- Amyloid-beta blocks Nr4a2 activation, leading to synaptic dysfunction in the hippocampus.
- Nr4a2 levels are reduced in early Alzheimer's disease human brain tissue samples.
- Pharmacological activation of Nr4a2 prevents synaptic depression caused by amyloid-beta.
- Overexpressing Nr4a2 improves spatial memory deficits in Alzheimer's mouse models.
PROKR1-CREB-NR4A2 axis for oxidative muscle fiber specification and improvement of metabolic function.
Mok J, Park JH, Yeom SC, Park J
This study identifies a biological pathway in muscle tissue where activating PROKR1 increases NR4A2 levels to improve metabolic health and muscle fiber type. The findings are based entirely on mouse models and cell cultures, with no evidence of human application or clinical relevance for NR4A2-related neurological syndromes.
- The research focuses exclusively on skeletal muscle metabolism and fiber composition.
- NR4A2 acts downstream of PROKR1 to promote oxidative muscle fibers in mice.
- No human data, clinical trials, or neurological phenotypes are reported.
- The mechanism is unrelated to the dopaminergic pathways affected in NR4A2 syndromes.
Identifying novel gene dysregulation associated with opioid overdose death: A meta-analysis of differential gene expression in human prefrontal cortex.
Carter JK, Quach BC, Willis C, Minto MS, PGC-SUD Epigenetics Working Group, Hancock DB, Montalvo-Ortiz J, Corradin O, Logan RW, Walss-Bass C, Maher BS, Johnson EO
This study identifies NR4A2 as one of many genes with altered expression in the brains of individuals who died from opioid overdose, but it does not establish a causal link to NR4A2-related syndrome or provide treatment insights. The findings reflect broad changes in neuronal plasticity and signaling pathways associated with opioid toxicity rather than specific genetic mechanisms of NR4A2 disorders. Consequently, this research offers no direct clinical guidance for managing NR4A2-related conditions.
- NR4A2 shows altered expression in postmortem brains of opioid overdose victims.
- The study analyzes human prefrontal cortex tissue from 285 individuals.
- Changes link to neuronal plasticity and signaling pathways like MEK/ERK/MAPK.
- No evidence suggests genetic drivers cause these specific expression differences.
- Findings relate to opioid toxicity mechanisms, not NR4A2 syndrome pathology.
Characteristics of the synovial microenvironment and synovial mesenchymal stem cells with hip osteoarthritis of different bone morphologies.
Yang Y, Koga H, Nakagawa Y, Nakamura T, Katagiri H, Takada R, Katakura M, Tsuji K, Sekiya I, Miyatake K
In hip osteoarthritis, the hypertrophic bone type is linked to increased activity of AP-1 family genes in the synovium and higher levels of inflammatory proteins like CXCL8, MMP9, and VEGF in joint fluid, which may drive abnormal bone growth and worsen joint damage.
- AP-1 genes are overactive in hypertrophic hip osteoarthritis
- Synovial fluid has more inflammatory proteins in hypertrophic cases
- These proteins may promote bone growth and joint damage
- SMSCs show no major differences in potential between groups
- SOX9 is elevated, suggesting cartilage-related activity
Gene architecture is a determinant of the transcriptional response to bulky DNA damages.
Merav M, Bitensky EM, Heilbrun EE, Hacohen T, Kirshenbaum A, Golan-Berman H, Cohen Y, Adar S
This study identifies NR4A2 as a gene that remains active during cellular stress caused by DNA damage, suggesting it plays a role in the body's repair mechanisms. The research focuses on general molecular biology and does not provide information specific to NR4A2-related syndromes or potential treatments for children.
- NR4A2 expression increases when cells face bulky DNA damage from UV, chemotherapy, or smoke components.
- Gene length and GC content determine how much a gene's activity drops during DNA stress.
- Active genes like NR4A2 undergo faster repair, allowing quicker restoration of normal function.
- The study highlights general genome architecture rules rather than specific disease mechanisms.
Investigating In silico and In vitro Therapeutic Potential of Diosmetin as the Anti-Parkinson Agent.
Varshney KK, Gupta JK, Srivastava R
Computer modeling and cell tests show that the plant compound diosmetin binds to NURR1 (NR4A2) and other proteins involved in oxidative stress. This interaction suggests potential antioxidant effects, but no human or animal studies confirm whether this compound helps Parkinson's disease or NR4A2-related conditions.
- Diosmetin binds to NURR1 in computer models with high affinity.
- The compound shows antioxidant activity against free radicals in lab tests.
- No human clinical data or animal efficacy studies are reported.
- This is purely preclinical molecular biology research.
Structural Perspective of NR4A Nuclear Receptor Family and Their Potential Endogenous Ligands.
Hashida R, Kawabata T
This study uses computer modeling to predict how potential natural ligands bind to NR4A1 and NR4A3 based on known structures of NR4A2. It does not provide new clinical data or direct treatment insights for patients with NR4A2-related syndromes.
- Researchers modeled binding structures for NR4A1 and NR4A3 using existing NR4A2 data.
- The paper reviews ligand-binding mechanisms within the broader nuclear receptor family.
- No human clinical trials or patient outcome data are included in this work.
Structurally Distinct Nurr1 Ligands Exhibit Different Pharmacological Characteristics in Regulating Inflammatory Responses of Microglial BV-2 Cells.
Nakanishi R, Kurauchi Y, Kotani S, Hitora-Imamura N, Seki T, Katsuki H
Three different compounds that activate the NR4A2 protein reduce inflammation in microglial brain cells, but they achieve this through distinct and sometimes opposing mechanisms. One compound specifically blocks a key inflammatory signal, while another suppresses specific inflammatory genes, suggesting that not all NR4A2 activators work the same way.
- Three NR4A2 ligands reduce inflammation in microglial cells.
- Each compound uses a different mechanism to inhibit inflammatory signals.
- Some effects of one drug are cancelled out by another.
- This study uses cell lines, not human patients or animals.
Transcriptional profiling of Kiss1 neurons from arcuate and rostral periventricular hypothalamic regions in female mice.
Manchishi S, Prater M, Colledge WH
This study maps the genetic differences between two types of kisspeptin-producing neurons in female mice to understand their roles in fertility. It identifies specific genes, including NR4A2, that are expressed differently in these neuronal populations. The findings provide basic molecular data on neuron subtypes but do not address human disease or treatment.
- Researchers compared gene expression in two kisspeptin neuron groups in female mice.
- The study identified hundreds of genes with different activity levels between the groups.
- NR4A2 is listed as a gene expressed in one specific kisspeptin neuron population.
- The work focuses on basic reproductive biology and neuronal molecular signatures.
- No human patients, clinical outcomes, or therapeutic strategies are evaluated.
Natural products and synthetic analogs as selective orphan nuclear receptor 4A (NR4A) modulators.
Safe S
This paper catalogs various natural and synthetic compounds that bind to NR4A receptors, including Nurr1 (NR4A2), but it does not test any treatments in humans or animal models of disease. The research focuses on identifying these chemical interactions for potential future drug development rather than providing clinical evidence or therapeutic guidance for NR4A2-related syndromes.
- The study identifies natural products and synthetic analogs that bind NR4A receptors.
- It highlights selective modulation of NR4A1, NR4A2, and NR4A3 by specific compounds.
- No human clinical data or disease model results are presented.
- The work serves as a chemical inventory for future therapeutic development.
Application of OpenArray Technology to Assess Changes in the Expression of Functionally Significant Genes in the Substantia Nigra of Mice in a Model of Parkinson's Disease.
Troshev D, Kolacheva A, Pavlova E, Blokhin V, Ugrumov M
This study measures gene expression changes in the brains of mice with a Parkinson's disease model. It finds that Nr4a2 levels drop alongside other dopamine-related genes, suggesting impaired dopamine function and transport. The research provides no direct evidence for human treatment or NR4A2 syndrome management.
- Nr4a2 expression decreases in the substantia nigra of mice with Parkinson's disease.
- Other dopamine synthesis and transport genes also show reduced expression.
- The study uses an MPTP mouse model, not human patients or NR4A2 variants.
- Results indicate impaired dopaminergic neuron function and antioxidant systems in mice.
Correction to: Adeno-associated virus (AAV) 9-mediated gene delivery of Nurr1 and Foxa2 ameliorates symptoms and pathologies of Alzheimer disease model mice by suppressing neuro-inflammation and glial pathology.
Yang Y, Seok MJ, Kim YE, Choi Y, Song JJ, Sulistio YA, Kim SH, Chang MY, Oh SJ, Nam MH, Kim YK, Kim TG, Im HI, Koh SH, Lee SH
This study demonstrates that delivering Nurr1 and Foxa2 genes via AAV9 reduces neuro-inflammation and glial pathology in mice with Alzheimer's disease. The treatment ameliorates behavioral symptoms and pathological markers associated with the condition in this animal model.
- AAV9 delivers Nurr1 and Foxa2 genes to mouse brains.
- Treatment suppresses neuro-inflammation and glial pathology.
- Alzheimer's disease symptoms improve in the mouse model.
- Results are preclinical and do not involve human participants.
Correction: Adeno-associated virus (AAV) 9-mediated gene delivery of Nurr1 and Foxa2 ameliorates symptoms and pathologies of Alzheimer disease model mice by suppressing neuro-inflammation and glial pathology.
Yang Y, Seok MJ, Kim YE, Choi Y, Song JJ, Sulistio YA, Kim SH, Chang MY, Oh SJ, Nam MH, Kim YK, Kim TG, Im HI, Koh SH, Lee SH
Delivering Nurr1 and Foxa2 genes via a viral vector reduces inflammation and glial damage in mice with Alzheimer's disease. This approach improves symptoms and pathology in an animal model of neurodegeneration. The study does not involve human participants or NR4A2-related syndromes.
- The study uses Alzheimer's disease mouse models, not NR4A2 syndrome models.
- Gene therapy targets Nurr1 and Foxa2 to suppress neuro-inflammation.
- Results show reduced glial pathology and improved symptoms in mice.
- No human clinical data or relevance to NR4A2 variants is presented.
(-)-Epigallocatechin-3-gallate promotes intestinal epithelial proliferation and barrier function after ischemia/reperfusion injury via activation of Nurr1.
Gao J, Wang Y, Jia Z, Xue J, Zhou T, Zu G
EGCG, a compound found in green tea, restores intestinal barrier function and promotes cell growth after injury by activating the Nurr1 protein. This protective effect disappears when Nurr1 is blocked, confirming that Nurr1 mediates these benefits.
- EGCG improves intestinal healing and barrier integrity in rats after ischemia-reperfusion injury.
- The benefit depends on Nurr1 activation, as blocking Nurr1 stops the protective effect.
- This study focuses on gut tissue repair, not neurological or dopaminergic outcomes.
Bioinformatics analysis and machine learning approach applied to the identification of novel key genes involved in non-alcoholic fatty liver disease.
Nazari E, Khalili-Tanha G, Asadnia A, Pourali G, Maftooh M, Khazaei M, Nasiri M, Hassanian SM, Ghayour-Mobarhan M, Ferns GA, Kiani MA, Avan A
This study used machine learning to analyze gene expression in fatty liver disease and identified NR4A2 as a potential diagnostic marker. The findings suggest NR4A2 levels may help detect early liver fat buildup, but the research focuses on liver disease, not NR4A2-related neurodevelopmental syndrome.
- NR4A2 was identified as a potential diagnostic marker for fatty liver disease
- The study used machine learning and patient data from public databases
- Other genes like ABCF1 and SART3 were also linked to fatty liver
- Findings are specific to liver disease, not neurological or developmental aspects
- No direct relevance to NR4A2-related neurodevelopmental disorders
The Promotion of Humoral Immune Responses in Humans via SOCS1-Mediated Th2-Bias Following SARS-CoV-2 Vaccination.
Liu X, Han J, Cui R, Peng M, Song H, Li R, Chen G
This study identifies NR4A2 as a biomarker associated with antibody production following SARS-CoV-2 vaccination in humans. It does not provide information on the neurodevelopmental or motor symptoms characteristic of NR4A2-related syndromes.
- NR4A2 expression correlates with serum antibody levels after COVID-19 vaccination.
- The research focuses on immune response mechanisms, not neurological development.
- No findings relate to the clinical phenotype or treatment of NR4A2 syndrome.
Compensatory Processes in Striatal Neurons Expressing the Tyrosine Hydroxylase Gene in Transgenic Mice in a Model of Parkinson's Disease.
Troshev D, Bannikova A, Blokhin V, Pavlova E, Kolacheva A, Ugrumov M
Parkinsonian mice increase the production of dopamine in specific striatal neurons to compensate for nerve damage. This study identifies Nurr1 and other genes as key drivers of this compensatory mechanism, suggesting that supporting these pathways could help maintain motor function.
- MPTP-treated mice show a 1.9-fold increase in dopamine-producing striatal neurons.
- Nurr1 gene expression rises 2.5-fold alongside tyrosine hydroxylase in these animals.
- Dopamine synthesis shifts from nerve fibers to neuronal cell bodies during compensation.
- The findings suggest maintaining dopamine homeostasis may improve Parkinson's treatment.