Development of In Vitro Parkinson's Disease Model Mediated by MPP+ and α-Synuclein Using Wharton's Jelly Mesenchymal Stem Cells.
Gamit N, Patil M, Soumya BS, Dharmarajan A, Warrier S
This study creates a laboratory model of Parkinson's disease using stem cells to mimic the loss of dopaminergic neurons. It demonstrates that toxic agents can reduce Nurr1 levels and cause cell death in these cells, providing a tool for drug screening. This work does not provide clinical evidence or treatment options for NR4A2-related syndromes.
- Researchers differentiated stem cells into dopaminergic neurons expressing Nurr1.
- Toxic agents reduced Nurr1 expression and caused neuronal cell death in the model.
- The model serves as a cost-effective tool for screening potential Parkinson's therapies.
- No human patients or NR4A2 genetic variants were studied in this research.
Satb2 and Nr4a2 are required for the differentiation of cortical layer 6b.
Zhao L, Tao YC, Hu L, Liu XY, Zhang Q, Zhang L, Ding YQ, Song NN
This study uses mouse models to show that the Nr4a2 protein works alongside Satb2 to help specific early-born neurons in the cerebral cortex develop correctly. Deleting Nr4a2 disrupts this developmental process, confirming its essential role in forming cortical layer 6b neurons during brain growth.
- Nr4a2 and Satb2 cooperate to drive the differentiation of early-born cortical neurons.
- Deleting Nr4a2 alters gene expression patterns required for normal layer 6b development.
- Satb2 deletion increases Nr4a2 levels, suggesting complex regulatory interactions between these factors.
- The research relies entirely on mouse models and does not involve human patients or treatments.
Mitigating Diabetic Cardiomyopathy: The Synergistic Potential of Sea Buckthorn and Metformin Explored via Bioinformatics and Chemoinformatics.
Safavi K, Abedpoor N, Hajibabaie F, Kaviani E
This study found that combining sea buckthorn extract and metformin works better than either treatment alone in protecting the hearts of mice with diabetes-related heart disease. The combination reduced inflammation, oxidative stress, and cell death in the heart, partly by regulating genes like NR4A2 that are involved in ferroptosis and metabolic health.
- Sea buckthorn and metformin together protect the heart in diabetic mice
- NR4A2 is among key genes involved in the heart damage process
- The combo reduces inflammation and cell death more effectively than single treatments
- Targeting ferroptosis may help treat diabetic heart disease
- Results suggest a promising new approach for managing heart complications in diabetes
Increased NaV1.2 expression and its interaction with CaM contribute to the hyperexcitability induced by prolonged inhibition of CaMKII.
Liang H, Qin L, Feng R, Shim J, Huang X, Xu X, Zhao D, Yu Z, Boczek T, Li M, Tong Y, Huang J, Gao Q, Wang L, Cao X, Liu D, Du K, Xu J, Zhao Y, Wang W, Seehus CR, Zhao W, Guo F
Inhibiting the enzyme CaMKII in neurons causes hyperexcitability and seizure-like activity by reducing NR4A2 levels, which leads to an overexpression of the sodium channel NaV1.2. This excessive sodium channel activity is driven by increased binding between NaV1.2 and calmodulin, a process that can be reversed by blocking this specific interaction.
- CaMKII inhibition reduces NR4A2 expression in neurons from rats, mice, and humans.
- Lower NR4A2 levels cause increased production of the NaV1.2 sodium channel.
- Excess NaV1.2 binds more strongly to calmodulin, increasing neuronal excitability.
- Blocking the NaV12-calmodulin interaction rescues hyperexcitability in experimental models.
Towards a unified molecular mechanism for liganddependent activation of NR4A-RXR heterodimers.
Yu X, He Y, Kamenecka TM, Kojetin DJ
This study identifies a specific molecular mechanism where certain ligands cause the NR4A2 protein complex to dissociate, potentially offering a new way to target these proteins in disease. The findings suggest that current drug testing methods may need expansion to capture this alternative activation pathway. This work remains strictly at the basic science level with no direct clinical application or human data.
- Ligands can trigger NR4A2-RXR dissociation, a non-classical activation mechanism.
- Selective agonists are required to observe this dissociation effect clearly.
- The study proposes unifying this mechanism for neurodegenerative disease targeting.
- No human trials, patient data, or clinical treatments are involved.
Neurotoxic Effects of Atrazine on Dopaminergic System via miRNAs and Energy-Sensing Pathways.
Chen X, Hu X, Liu H, He J, Li Y, Zhang X
Atrazine exposure damages the dopaminergic system in rats by reducing key proteins like NURR1 and tyrosine hydroxylase while increasing alpha-synuclein. The study identifies specific microRNA and energy-sensing pathway changes that drive this neurotoxicity.
- Atrazine lowers NURR1 and tyrosine hydroxylase levels in rat brains.
- Atrazine increases alpha-synuclein, a protein linked to neuronal stress.
- The herbicide alters miRNA profiles affecting dopaminergic development.
- AMPK and mTOR pathways show significant changes during exposure.
- Findings suggest mechanisms for preventing atrazine-induced neurotoxicity.
The Organogermanium Compound 3-(trihydroxygermyl)propanoic Acid Exerts Anti-Inflammatory Effects via Adenosine-NR4A2 Signaling.
Azumi J, Takeda T, Shibata S, Shimada Y, Aso H, Nakamura T
This study identifies a mechanism where an organogermanium compound reduces inflammation by stabilizing adenosine to activate the NR4A2 pathway in immune cells. The findings are based entirely on cell culture experiments and do not involve human patients or animal models of neurological disease.
- The research uses THP-1 immune cells, not neurons or patient samples.
- It focuses on general inflammation suppression via NR4A2 signaling.
- No evidence is provided for treating NR4A2-related syndromes in humans.
- The compound targets inflammatory pathways unrelated to dopaminergic function.
NURR1 Deficiency Is Associated to Altered Microglial Phenotype in Male Mice.
Montarolo F, Thielens S, Bove M, Bertolotto A, Tempia F, Hoxha E
NURR1 deficiency in male mice reduces the number of microglial cells in the substantia nigra and alters their inflammatory gene expression without affecting dopamine neuron survival. These specific changes in brain immune cells correlate with the hyperactive and impulsive behaviors observed in the deficient mice.
- NURR1 loss lowers microglial cell counts specifically in the substantia nigra region of the brain.
- Inflammatory gene markers shift, indicating altered stress response and cellular damage signaling.
- Dopamine neuron numbers remain normal despite the behavioral changes and immune alterations.
- The study links NURR1's role in microglia directly to behavioral outcomes in mice.
Effects of culture media on gene expression in reconstructed human epidermis and THP-1 monocytes for skin sensitization evaluation in co-culture systems.
Sugimoto-Sawada Y, Yamashiro M, Kono M, Ikeda H, Itagaki H, Iijima K
The study found that NR4A2 and other genes (NR4A1, NR4A3, SIK1, HMOX1) are more strongly activated in immune cells when skin cells are exposed to a skin sensitizer, suggesting these genes could help detect skin allergies. The type of culture medium had a bigger effect on gene activity than cell-to-cell contact, but the interaction between skin and immune cells still influenced responses to irritants.
- NR4A2 increases in immune cells when skin cells are exposed to a sensitizer
- Five genes (NR4A1, NR4A2, NR4A3, SIK1, HMOX1) are strong markers for skin sensitization
- Culture medium affects gene expression more than cell co-culture
- Skin cell damage signals boost immune cell gene activity
- These genes may help detect skin allergies in testing
Transcriptomic analysis of chronic chikungunya in the Reunionese CHIKGene cohort uncovers a shift in gene expression more than 10 years after infection.
Gérardin P, Medina-Santos R, Le Clerc S, Bruneau L, Maillot A, Labib T, Rahmouni M, Spadoni JL, Meyniel JP, Cornet C, Lefebvre C, El Jahrani N, Savara J, Mathew MJ, Fontaine C, Payet C, Ah-You N, Chabert C, Mussard C, Porcherat S, Medjane S, Noirel J, Marimoutou C, Hocini H, Zagury JF
This study found long-term changes in gene activity in people still suffering from chikungunya symptoms over 10 years after infection, including genes linked to immune function, nerve health, and cell metabolism. These changes suggest ongoing immune and neurological issues, possibly due to a hidden virus or increased vulnerability to other infections.
- Gene changes persist over 10 years after chikungunya infection
- Immune and nerve-related genes are significantly altered
- Findings suggest possible hidden virus or immune dysfunction
- May point to new treatment targets for chronic symptoms
Modeling amyotrophic lateral sclerosis with amniotic membrane-derived mesenchymal stem cells: A novel approach for disease modeling.
Soumya BS, Gamit N, Patil M, Shreenidhi VP, Dharmarajan A, Warrier S
This study creates an in-vitro model of ALS using stem cells to screen for drugs, rather than investigating NR4A2-related syndromes. The researchers induced ALS-like symptoms in motor neurons and observed that the NURR1 gene expression increased alongside oxidative stress. This work provides a platform for drug testing in ALS but offers no direct insights into treatment or mechanisms for NR4A2 conditions.
- The study models ALS, not NR4A2-related syndromes or Parkinson's disease.
- NURR1 expression rises as a secondary effect of induced oxidative stress in this model.
- No human data, clinical trials, or specific NR4A2 therapies are evaluated.
- The findings apply to general ALS drug screening, not the child's condition.
Identification of NR4A2 as a Potential Predictive Biomarker for Atherosclerosis.
Yuan L, Bai R, Han X, Xiang J
NR4A2 is elevated in atherosclerotic plaques and strongly linked to immune cells involved in the disease, suggesting it could help diagnose or monitor atherosclerosis. This finding highlights NR4A2 as a potential biomarker for a common cardiovascular condition.
- NR4A2 levels rise in atherosclerotic plaques
- NR4A2 correlates with immune cells like macrophages and B cells
- Machine learning identified NR4A2 as a top candidate biomarker
- Validation confirmed higher NR4A2 in disease tissue
- May help diagnose or track atherosclerosis progression
Embryonic exposure to valproic acid and neonicotinoid deteriorates the hyperpolarizing GABA shift and impairs long-term potentiation of excitatory transmission in the local circuit of intermediate medial mesopallium of chick telencephalon.
Matsushima T, Toji N, Wada K, Shikanai H, Izumi T
Exposure to valproic acid or imidacloprid during embryonic development disrupts normal brain circuitry and impairs learning in chicks. These chemicals downregulate NR4A2 along with other transcriptional regulators, leading to impaired synaptic plasticity that can be partially rescued by specific ion channel blockers.
- Embryonic exposure to valproic acid or imidacloprid impairs learning and memory in chicks.
- These exposures disrupt GABA signaling and impair long-term potentiation in brain circuits.
- Both chemicals downregulate NR4A2 and other transcriptional regulators in the developing brain.
- Bumetanide rescues impaired synaptic plasticity caused by valproic acid exposure.
- The study uses chick models to investigate environmental impacts on neurodevelopment.
Celecoxib Enhances Oxidative Muscle Fibre Formation and Improves Muscle Functions Through Prokr1 Activation in Mice.
Park JH, Mok J, Park S, Kim D, Kang MS, Park TS, Park J
This study shows that celecoxib improves muscle strength and metabolism in mice by activating a specific receptor pathway. The research focuses entirely on skeletal muscle physiology and does not address the dopaminergic neuron loss or movement disorders associated with NR4A2-related syndromes.
- Celecoxib activates PROKR1 signaling to increase oxidative muscle fibers in mice.
- Prenatal celecoxib exposure improves lean mass and grip strength in offspring.
- The drug enhances mitochondrial content and fatty acid oxidation in muscle tissue.
- NR4A2 levels rise as a downstream effect of PROKR1 activation in this context.
- The study investigates skeletal muscle, not the brain pathways affected by NR4A2.
Discovery of Endothelial-Monocyte Crosstalk in Ischemic-Reperfusion Injury Following Liver Transplantation Based on Integration of Single-Cell RNA and Transcriptome RNA Sequencing.
Sun C, Li L, Li D, Wang Z
This study investigates liver injury during transplantation and identifies NR4A2 as a gene upregulated in immune cells called monocytes. The research focuses on how these immune cells interact with liver blood vessel cells to worsen inflammation, using patient data and mouse models. It does not address brain development, neurological symptoms, or potential treatments for NR4A2-related syndromes.
- NR4A2 appears in monocytes during liver ischemia-reperfusion injury, not in neural contexts.
- The study links NR4A2 to immune-mediated inflammation in the liver.
- Findings rely on mouse models and human liver tissue, not neurological phenotypes.
- No connection is made to dopaminergic neurons or neurodevelopmental outcomes.
Contribution of the dopaminergic system in toxoplasmic encephalitis neuroimmunopathogenesis.
Anteplıoğlu T, Dincel GC, Alçiğir ME, Bışkın Türkmen M, Yapici TS, Kul O, Al-Olayan E, Alshahrani MY, El-Ashram S
This study examines how a parasitic brain infection alters dopamine-related proteins in mice, finding that while one production enzyme increases, key receptors and transporters decrease. The research focuses on the biological mechanisms of toxoplasmic encephalitis rather than NR4A2-related genetic syndromes or human clinical outcomes.
- The study uses infected mice, not humans or patients with NR4A2 variants.
- It investigates Toxoplasma gondii infection, a parasitic disease unrelated to genetic neurodevelopmental disorders.
- Findings describe protein expression changes in mouse brain tissue during chronic infection.
- No clinical data, treatment trials, or genotype-phenotype correlations for NR4A2 are presented.
Luteolin ameliorates rat model of metabolic syndrome-induced cardiac injury by apoptosis suppression and autophagy promotion via NR4A2/p53 regulation.
Dai X, Liang B, Sun Y
Luteolin protects rat hearts from metabolic syndrome damage by regulating NR4A2 to reduce cell death and improve cellular cleanup. This study uses an animal model of heart disease, not a human condition related to NR4A2 syndromes.
- Study tests luteolin in rats with metabolic syndrome, not NR4A2-related disorders.
- NR4A2 regulates heart cell survival and cleanup pathways in this animal model.
- Luteolin reduces inflammation and stress markers in rat hearts.
- No human data or direct link to NR4A2 genetic syndromes is provided.
Overexpression of FTO alleviates traumatic brain injury induced posttraumatic epilepsy by upregulating NR4A2 expression via m6A demethylation.
Xiao M, Wang X, Xiao E, Ming Q
This study shows that increasing FTO protein levels reduces epilepsy and brain damage in mice after traumatic brain injury by stabilizing NR4A2 mRNA. The mechanism involves FTO removing methyl groups from NR4A2, which prevents its degradation and allows it to protect neurons.
- FTO overexpression reduces seizure frequency and neuronal damage in mouse models of post-traumatic epilepsy.
- FTO upregulates NR4A2 by removing m6A marks, preventing the mRNA from being degraded.
- Blocking NR4A2 reverses the protective effects of FTO, confirming it is a key downstream target.
- The findings suggest targeting the FTO-NR4A2 axis could treat epilepsy following brain injury.
Bioinformatics-driven identification and validation of hub genes regulating endometriosis-related infertility within human granulosa cells.
Luo J, Wang H, Zhou L, Wang J, Song M, Cheng Y, Rao M, Zhao S, Tang L
This study identifies NR4A2 as one of five hub genes in human granulosa cells associated with endometriosis-related infertility, but it does not investigate its role in neurodevelopment or motor function. The research focuses on using BTG2, another identified gene, as a biomarker for predicting oocyte quality and IVF outcomes rather than addressing the child's condition.
- NR4A2 is identified as a hub gene in granulosa cells from patients with endometriosis.
- The study links BTG2 expression levels to oocyte retrieval rates and blastocyst formation.
- No findings relate to NR4A2's function in the brain, dopamine pathways, or motor control.
- The research is limited to reproductive biology and infertility outcomes.
Unveiling the Therapeutic Potential of Small Molecule of SVAK-12: A Comprehensive In Silico, In Vitro, and In Vivo Studies on its Neuroprotective Effects and Molecular Interactions in Parkinson's Disease.
Kokabi S, Amiri M, Alahdad N, Yazdanpanah MA, Shahbazi A, Barati M, Simorgh S, Azedi F, Angaji SA, Tavakol S
SVAK-12 is a small molecule that protects brain cells in models of Parkinson’s disease by reducing oxidative stress, boosting brain-derived growth factors, and increasing dopamine levels. It shows strong potential as a neuroprotective treatment, though it did not improve motor symptoms in animal models.
- SVAK-12 reduces brain cell damage and oxidative stress
- Increases BDNF and GDNF, supporting neuron survival
- Boosts dopamine and tyrosine hydroxylase levels
- Crosses the blood-brain barrier and remains stable
- Shows strong binding to key neuroprotective receptors
WITHDRAWN: Overexpression of NR4A2 Alleviates Renal and Myocardial Injury in Diabetic Nephropathy in Rats Through the HDAC11/ SPRY1 Pathway.
Xu J, Li J, Xu X, Zhu H, Zhang X, Yang M, Ren Y
This paper has been withdrawn and is not available for review. No reliable data or conclusions can be provided.
- The study was withdrawn by the publisher
- No valid results or findings are available
- The paper cannot be used for clinical or research decisions
JMJD3 deficiency disturbs dopamine biosynthesis in midbrain and aggravates chronic inflammatory pain.
He XB, Guo F, Zhang W, Fan J, Le W, Chen Q, Ma Y, Zheng Y, Lee SH, Wang HJ, Wu Y, Zhou Q, Yang R
JMJD3 deficiency reduces dopamine levels in the midbrain of mice by suppressing the expression of NURR1 and tyrosine hydroxylase. This molecular disruption leads to prolonged chronic inflammatory pain without affecting motor function.
- JMJD3 is required for normal dopamine biosynthesis in adult mouse midbrain neurons.
- Loss of JMJD3 decreases NURR1 and TH protein levels via epigenetic suppression.
- Mice with reduced JMJD3 activity exhibit prolonged inflammatory pain sensitivity.
- Motor function remains intact despite significant reductions in dopamine content.
Canagliflozin attenuates neurodegeneration and ameliorates dyskinesia through targeting the NLRP3/Nurr1/GSK-3β/SIRT3 pathway and autophagy modulation in rotenone-lesioned rats.
Abdelaziz AM, Rasheed NOA, Zaki HF, Salem HA, El-Sayed RM
Canagliflozin reduces neurodegeneration and dyskinesia in a rat model of Parkinson's disease by modulating inflammatory and metabolic pathways involving Nurr1. This preclinical study demonstrates potential neuroprotective effects but does not provide evidence for efficacy or safety in humans.
- Study uses rotenone-lesioned rats, not human patients or NR4A2-specific models.
- Canagliflozin improves motor symptoms and reduces inflammation in the animal model.
- Mechanism involves modulation of Nurr1, GSK-3β, and autophagy pathways.
- No clinical data exists for this drug in treating NR4A2-related syndromes.
Implication of Pyrethroid Neurotoxicity for Human Health: A Lesson from Animal Models.
Oyovwi MO, Atere AD, Chimwuba P, Joseph UG
Pyrethroid insecticides can cause neurological damage by disrupting ion channels, increasing oxidative stress and inflammation, impairing mitochondria, and altering gene expression through epigenetic changes. These effects mimic pathways seen in neurodegenerative diseases and may interfere with key protective brain pathways like Nurr1 and Nrf2.
- Pyrethroids harm the nervous system through multiple toxic pathways
- Oxidative stress and inflammation are major drivers of neuronal damage
- Mitochondrial and ion channel dysfunction contribute to neurodegeneration
- Epigenetic changes may increase risk for neurological disorders
- Nurr1 and other protective pathways may be impaired by exposure
Establishment and validation of diagnostic model in immunoglobulin A nephropathy based on weighted gene co-expression network analysis.
Liu H, Dai L, Liu J, Duan K, Yi F, Li Z
This study developed a 5-gene diagnostic model for IgA nephropathy with high accuracy, using gene expression data from kidney tissue. The model can reliably distinguish IgAN patients from healthy individuals and may help guide diagnosis and treatment.
- A 5-gene panel accurately diagnoses IgA nephropathy
- Model has high accuracy (AUC of 0.964)
- Genes in the model are linked to immune and kidney function
- Model was validated in independent patient data
- Could support earlier and more precise diagnosis
NR4A1 and NR4A2 orphan nuclear receptors regulate endothelial-to-hematopoietic transition in mouse hematopoietic stem cell specification.
Sá da Bandeira D, Nevitt CD, Segato Dezem F, Marção M, Liu Y, Kelley Z, DuBose H, Chabot A, Hall T, Caprio C, Okhomina V, Kang G, Plummer J, McKinney-Freeman S, Clements WK, Ganuza M
This study shows that NR4A1 and NR4A2 genes are essential for the development of blood stem cells in mice by regulating a specific signaling pathway. The research identifies a mechanism where these genes help blood stem cells mature, but it does not involve dopaminergic neurons or Parkinson's disease.
- NR4A1 and NR4A2 regulate blood stem cell development in mouse embryos.
- Loss of these genes blocks the maturation of hematopoietic stem cells.
- The mechanism involves Notch signaling regulation during endothelial-to-hematopoietic transition.
- This work focuses on blood formation, not brain or dopamine pathways.
The endocannabinoid anandamide mediates anti-inflammatory effects through activation of NR4A nuclear receptors.
Teichmann T, Pflüger-Müller B, Giménez VMM, Sailer F, Dirks H, Zehr S, Warwick T, Brettner F, Munoz-Tello P, Zimmer A, Tegeder I, Thomas D, Gurke R, Günther S, Heering J, Proschak E, Geisslinger G, Bibli IS, Heringdorf DMZ, Manucha W, Windbergs M, Knapp S, Weigert A, Leisegang MS, Kojetin D, Brandes RP
This study shows that the endocannabinoid anandamide reduces inflammation in blood vessel cells by directly binding to and activating NR4A nuclear receptors. This mechanism suppresses inflammatory genes through a pathway unrelated to dopaminergic neurons or movement disorders.
- Anandamide activates NR4A1 and NR4A2 receptors to block inflammatory gene expression.
- The effect occurs in vascular smooth muscle cells, not brain tissue.
- NR4A mutations reduce anandamide binding, confirming direct receptor interaction.
- This research focuses on cardiovascular inflammation, not neurological symptoms.
RNA-binding protein biomarkers NR4A2 and NR4A3 in renal ischemia-reperfusion injury diagnosis.
Chen J, Chen X, Zhang K
NR4A2 and NR4A3 are highly expressed in kidney injury after reduced blood flow and restored circulation, making them potential blood or urine tests to detect this type of kidney damage. These proteins are linked to brain-related signaling pathways and are regulated by noncoding RNAs and other genes, with several drugs predicted to affect them.
- NR4A2 and NR4A3 are strong biomarkers for kidney injury after blood flow disruption
- They are consistently elevated in two independent kidney injury datasets
- They are regulated by noncoding RNAs and transcription factors
- Drug predictions suggest possible treatments targeting these proteins
- May help diagnose kidney injury in transplant patients
Analysing the gene expression profiles of the orphan nuclear receptors NR4A1, NR4A2 and NR4A3 in premalignant lesions of the cervix and cervicitis.
Cruz-Nieves RP, Ramírez-Rosales GE, González-Ramírez J, Sánchez-Muñoz F, Ruiz-Hernández A
This study found that NR4A2 levels change in cervical precancerous lesions, suggesting a possible role in early cancer development. However, the research focuses on cervical cancer in adults, not on NR4A2-related neurodevelopmental disorders in children.
- NR4A2 was detected in cervicitis and CIN III lesions
- NR4A2 expression varied with lesion severity
- Findings are from cervical cancer research, not neurodevelopmental conditions
- No direct relevance to NR4A2 syndrome in children
- No therapeutic implications for pediatric NR4A2-related disorders
OTUD7B inhibited hepatic injury from NAFLD by inhibiting K48-linked ubiquitination and degradation of β-catenin.
Sun J, Jin X, Li Y
This study shows that NR4A2 regulates the expression of OTUD7B, a protein that protects liver cells from damage and fat accumulation in mice with fatty liver disease. The research demonstrates a molecular link between NR4A2 and liver health mechanisms involving beta-catenin stabilization, but it does not test any treatments or observe human patients. This work provides background on NR4A2's biological function rather than actionable clinical information for your child.
- NR4A2 directly binds to and increases OTUD7B gene expression in liver cells.
- OTUD7B protects against fatty liver damage by stabilizing beta-catenin protein levels.
- The study uses mouse models and cell lines, not human participants.
- No clinical trials or patient outcomes are reported in this research.
Exploring Pathogenic Genes in Frozen Shoulder through weighted gene co-expression network analysis and Mendelian Randomization.
Wen D, Li B, Guo S, Chen L, Chen B
This study found that higher expression of four genes—ADAMTS1, NR4A2, PARD6G, and SMKR1—is likely to cause frozen shoulder. The genes were identified through genetic analysis and confirmed with lab tests, and they may help diagnose the condition.
- NR4A2 is linked to frozen shoulder risk
- Four genes may help diagnose frozen shoulder
- Higher gene expression increases disease risk
- Genetic analysis supports causal role
- Findings could guide future treatments
The Nr4a family regulates intrahepatic Treg proliferation and liver fibrosis in MASLD models.
Aki D, Hayakawa T, Srirat T, Shichino S, Ito M, Saitoh SI, Mise-Omata S, Yoshimura A
The Nr4a family of genes, including NR4A2, helps control immune cells in the liver that contribute to liver damage and scarring in metabolic liver disease. Removing Nr4a1 and Nr4a2 in immune cells boosts protective regulatory T cells (Tregs), reduces inflammation, and improves liver health in mouse models. This suggests that targeting NR4A2 could be a potential treatment strategy for liver disease.
- NR4A2 is involved in immune cell activity in the liver
- Blocking NR4A1/2 boosts protective Tregs
- This reduces liver damage and scarring in mice
- Tregs become more active and multiply in the liver
- Targeting NR4A2 may help treat liver disease