166 results match your criteria nrf2 bach1

Epigenetic Insights and Potential Modifiers as Therapeutic Targets in -Thalassemia.

Biomolecules 2021 May 18;11(5). Epub 2021 May 18.

Department of Haematology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian 16150, Malaysia.

Thalassemia, an inherited quantitative globin disorder, consists of two types, α- and -thalassemia. -thalassemia is a heterogeneous disease that can be asymptomatic, mild, or even severe. Considerable research has focused on investigating its underlying etiology. Read More

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Heme oxygenase-1 induction by heat shock in rat hepatoma cell line is regulated by the coordinated function of HSF1, NRF2, AND BACH1.

J Biochem 2021 Jun 1. Epub 2021 Jun 1.

Department of Pharmacy, Faculty of Pharmaceutical Sciences, Sanyo-Onoda City University 1-1-1 Daigakudohri, Sanyo-onoda-shi 756-0884, Japan.

The mechanism of heme oxygenase-1 (HO-1) induction by heat shock (HS) loading remains unclear. Here, we investigated the contribution of transcription factors to HS-induced HO-1 expression, using a rat hepatoma cell line (H-4-II-E). Our results demonstrated that HS treatment resulted in a marked induction of HO-1. Read More

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miR-380-5p facilitates NRF2 and attenuates cerebral ischemia/reperfusion injury-induced neuronal cell death by directly targeting BACH1.

Yibiao Wang Min Xu

Transl Neurosci 2021 Jan 18;12(1):210-217. Epub 2021 May 18.

Department of Neurosurgery, Kunshan Hospital of Traditional Chinese Medicine, Kunshan Affiliated Hospital of Nanjing University of Chinese Medicine, No. 189 Chaoyang Road, Kunshan City, Jiangsu Province, 215300, China.

Background: This study aimed to explore the role of miR-380-5p in cerebral ischemia/reperfusion (CIR) injury-induced neuronal cell death and the potential signaling pathway involved.

Methodology: Human neuroblastoma cell line SH-SY5Y cells were used in this study. Oxygen and glucose deprivation/reperfusion (OGD/R) model was used to mimic ischemia/reperfusion injury. Read More

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January 2021

The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging.

Oxid Med Cell Longev 2021 19;2021:6635460. Epub 2021 Apr 19.

Zunyi Municipal Key Laboratory of Medicinal Biotechnology, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Huichuan District, Zunyi 563003, China.

Oxidative stress, a term that describes the imbalance between oxidants and antioxidants, leads to the disruption of redox signals and causes molecular damage. Increased oxidative stress from diverse sources has been implicated in most senescence-related diseases and in aging itself. The Kelch-like ECH-associated protein 1- (Keap1-) nuclear factor-erythroid 2-related factor 2 (Nrf2) system can be used to monitor oxidative stress; Keap1-Nrf2 is closely associated with aging and controls the transcription of multiple antioxidant enzymes. Read More

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Challenges and Limitations of Targeting the Keap1-Nrf2 Pathway for Neurotherapeutics: Bach1 De-Repression to the Rescue.

Front Aging Neurosci 2021 8;13:673205. Epub 2021 Apr 8.

Darby Children's Research Institute, Medical University of South Carolina, Charleston, SC, United States.

The Keap1-Nrf2 signaling axis is a validated and promising target for cellular defense and survival pathways. This minireview discusses the potential off-target effects and their impact on future drug development originating from Keap1-targeting small molecules that function as displacement activators of the redox-sensitive transcription factor Nrf2. We argue that small-molecule displacement activators, similarly to electrophiles, will release both Nrf2 and other Keap1 client proteins from the ubiquitin ligase complex. Read More

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Expression of nuclear factor erythroid-2-related factor 2, broad complex-tramtrack-bric a brac and Cap'n'collar homology 1 and γ-glutamic acid cysteine synthase in peripheral blood of patients with chronic obstructive pulmonary disease and its clinical significance.

Exp Ther Med 2021 May 22;21(5):516. Epub 2021 Mar 22.

Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.

The purpose of the present study was to explore the relationship between nuclear factor erythroid 2-related factor 2 (Nrf2)/BTB-CNC allogeneic 1 (Bach1)/γ-glutamic acid cysteine synthase (γ-GCS) and chronic obstructive pulmonary disease (COPD). The expression of Nrf2, Bach1, γ-GCS mRNA and protein in the peripheral blood mononuclear cells (PBMCs) of 80 COPD patients and 40 healthy volunteers were studied. Then, the correlation between Nrf2, Bach1, γ-GCS and lung function, inflammation and oxidative stress indicators was analyzed. Read More

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A Novel Therapeutic Target, BACH1, Regulates Cancer Metabolism.

Cells 2021 Mar 12;10(3). Epub 2021 Mar 12.

Department of Biochemistry and Molecular Medicine, School of Medicine & Health Sciences, George Washington University, Washington, DC 20037, USA.

BTB domain and CNC homology 1 (BACH1) is a transcription factor that is highly expressed in tumors including breast and lung, relative to their non-tumor tissues. BACH1 is known to regulate multiple physiological processes including heme homeostasis, oxidative stress response, senescence, cell cycle, and mitosis. In a tumor, BACH1 promotes invasion and metastasis of cancer cells, and the expression of BACH1 presents a poor outcome for cancer patients including breast and lung cancer patients. Read More

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Pharmacological Targeting of Heme Oxygenase-1 in Osteoarthritis.

Antioxidants (Basel) 2021 Mar 9;10(3). Epub 2021 Mar 9.

Medical Center for Translational and Clinical Research, Hiroshima University Hospital, Hiroshima 7348551, Japan.

Osteoarthritis (OA) is a common aging-associated disease that clinically manifests as joint pain, mobility limitations, and compromised quality of life. Today, OA treatment is limited to pain management and joint arthroplasty at the later stages of disease progression. OA pathogenesis is predominantly mediated by oxidative damage to joint cartilage extracellular matrix and local cells such as chondrocytes, osteoclasts, osteoblasts, and synovial fibroblasts. Read More

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Crm1-Dependent Nuclear Export of Bach1 is Involved in the Protective Effect of Hyperoside on Oxidative Damage in Hepatocytes and CCl-induced Acute Liver Injury.

J Inflamm Res 2021 25;14:551-565. Epub 2021 Feb 25.

Department of Pharmacy, Daping Hospital, Army Medical University, Chongqing, 400042, People's Republic of China.

Background: Nrf2-Bach1 antioxidant signaling pathway is considered as one of the most important mechanisms of cellular resistance to oxidative injury. The effect of hyperoside (Hyp) on the expression and distribution of Bach1, the relationship of Hyp's antioxidative effect and the influence of Bach1 remains unclear.

Purpose: The aim of this study was to investigate the role and mechanisms of Bach1 in the protective effect of Hyp on oxidative liver injury. Read More

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February 2021

MiR-133a-3p relieves the oxidative stress induced trophoblast cell apoptosis through the BACH1/Nrf2/HO-1 signaling pathway.

H Guo Y Wang W Jia L Liu

Physiol Res 2021 03 14;70(1):67-78. Epub 2021 Jan 14.

Department of Obstetrics, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei, People's Republic of China.

Preeclampsia (PE) is a major cause of the pregnancy morbidity and mortality over the world. Disorganized placentation caused by trophoblast cell abnormity is one of main risk factors to induce PE. MiR-133a-3p has been shown to contain regulatory effects on oxidative stress in the cardiomyocytes. Read More

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Differential effects of arsenic species on Nrf2 and Bach1 nuclear localization in cultured hepatocytes.

Toxicol Appl Pharmacol 2021 02 9;413:115404. Epub 2021 Jan 9.

Environment and Non-Communicable Disease Research Center, Key Laboratory of Arsenic-related Biological Effects and Prevention and Treatment in Liaoning Province, School of Public Health, China Medical University, Shenyang, PR China. Electronic address:

Arsenic is a ubiquitous metalloid element present in both inorganic and organic forms in the environment. The liver is considered to be a primary organ of arsenic biotransformation and methylation, as well as the main target of arsenic toxicity. Studies have confirmed that Chang human hepatocytes have an efficient arsenic methylating capacity. Read More

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February 2021

Keap1-Nrf2 Pathway Regulates ALDH and Contributes to Radioresistance in Breast Cancer Stem Cells.

Cells 2021 Jan 6;10(1). Epub 2021 Jan 6.

Redox Biology Lab, National Centre for Cell Science (NCCS), Pune 411007, India.

Tumor recurrence after radiotherapy due to the presence of breast cancer stem cells (BCSCs) is a clinical challenge, and the mechanism remains unclear. Low levels of ROS and enhanced antioxidant defenses are shown to contribute to increasing radioresistance. However, the role of Nrf2-Keap1-Bach1 signaling in the radioresistance of BCSCs remains elusive. Read More

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January 2021

Age-related alteration in HNE elimination enzymes.

Arch Biochem Biophys 2021 03 5;699:108749. Epub 2021 Jan 5.

Leonard Davis School of Gerontology, University of Southern California, 3715 McClintock Avenue, Los Angeles, CA, 90089, United States. Electronic address:

4-hydroxynonenal (HNE, 4-hydroxy-2-nonenal) is a primary α,β-unsaturated aldehyde product of lipid peroxidation. The accumulation of HNE increases with aging and the mechanisms are mainly attributable to increased oxidative stress and decreased capacity of HNE elimination. In this review article, we summarize the studies on age-related change of HNE concentration and alteration of HNE metabolizing enzymes (GCL, GST, ALDHs, aldose reductase, and 20S-proteasome), and discuss potential mechanism of age-related decrease in HNE-elimination capacity by focusing on Nrf2 redox signaling. Read More

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Nrf2-induced miR-23a-27a-24-2 cluster modulates damage repair of intestinal mucosa by targeting the Bach1/HO-1 axis in inflammatory bowel diseases.

Free Radic Biol Med 2021 Feb 7;163:1-9. Epub 2020 Dec 7.

Department of Gastrointestinal Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, China. Electronic address:

IBD is an idiopathic, chronic autoimmune disease associated with intense oxidative stress. As a master modulator of oxidative stress, Nrf2 has an important anti-inflammatory role in colitis by activating HO-1 transcription. Meanwhile, HO-1 expression is transcriptionally suppressed by Bach1. Read More

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February 2021

Isomeric O-methyl cannabidiolquinones with dual BACH1/NRF2 activity.

Redox Biol 2020 10 22;37:101689. Epub 2020 Aug 22.

Jacqui Wood Cancer Centre, Division of Cellular Medicine, School of Medicine, University of Dundee, UK. Electronic address:

Oxidative stress and inflammation in the brain are two key hallmarks of neurodegenerative diseases (NDs) such as Alzheimer's, Parkinson's, Huntington's and multiple sclerosis. The axis NRF2-BACH1 has anti-inflammatory and anti-oxidant properties that could be exploited pharmacologically to obtain neuroprotective effects. Activation of NRF2 or inhibition of BACH1 are, individually, promising therapeutic approaches for NDs. Read More

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October 2020

Bach1 Inhibition Suppresses Osteoclastogenesis via Reduction of the Signaling via Reactive Oxygen Species by Reinforced Antioxidation.

Front Cell Dev Biol 2020 4;8:740. Epub 2020 Aug 4.

Department of Orthodontics, School of Dental Medicine, Tsurumi University, Yokohama, Japan.

Bone destructive diseases such as periodontitis are common worldwide and are caused by excessive osteoclast formation and activation. Receptor activator of nuclear factor-κB ligand (RANKL) is essential factor for osteoclastogenesis. This triggers reactive oxygen species (ROS), which has a key role in intracellular signaling as well exerting cytotoxicity. Read More

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The BACH1/Nrf2 Axis in Brain in Down Syndrome and Transition to Alzheimer Disease-Like Neuropathology and Dementia.

Antioxidants (Basel) 2020 Aug 21;9(9). Epub 2020 Aug 21.

Department of Chemistry University of Kentucky, Lexington, KY 40506, USA.

Down syndrome (DS) is the most common genetic cause of intellectual disability that is associated with an increased risk to develop early-onset Alzheimer-like dementia (AD). The brain neuropathological features include alteration of redox homeostasis, mitochondrial deficits, inflammation, accumulation of both amyloid beta-peptide oligomers and senile plaques, as well as aggregated hyperphosphorylated tau protein-containing neurofibrillary tangles, among others. It is worth mentioning that some of the triplicated genes encoded are likely to cause increased oxidative stress (OS) conditions that are also associated with reduced cellular responses. Read More

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Chronic PERK induction promotes Alzheimer-like neuropathology in Down syndrome: Insights for therapeutic intervention.

Prog Neurobiol 2021 01 11;196:101892. Epub 2020 Aug 11.

Department of Biochemical Sciences "A. Rossi Fanelli", Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome, Italy. Electronic address:

A major challenge in neurobiology is the identification of the mechanisms by which protein misfolding leads to cellular toxicity. Many neurodegenerative disorders, in which aberrant protein conformers aggregate into pathological inclusions, present the chronic activation of the PERK branch of the unfolded protein response. The adaptive effects of the PERK pathway include reduction of translation by transient inhibition of eIF2α and antioxidant protein production via induction of Nrf2 transcription factor. Read More

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January 2021

Dysregulation of hypoxia-inducible factor-1α (Hif1α) expression in the Hmox1-deficient placenta.

Placenta 2020 09 26;99:108-116. Epub 2020 Jul 26.

Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, 94305, USA.

Introduction: Severe hypoxia exists in placentas during early pregnancy, with reoxygenation during mid-gestation. Hypoxia-inducible factor-1α (Hif1α), an oxygen sensor, initiates placental vascular development. We have shown that the placental vasculature in Hmox1-deficient (Hmox1, Het) pregnancies is impaired, with morphological defects similar to Hif1α-deficient placentas. Read More

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September 2020

Hydroxyurea Scavenges Free Radicals and Induces the Expression of Antioxidant Genes in Human Cell Cultures Treated With Hemin.

Front Immunol 2020 17;11:1488. Epub 2020 Jul 17.

Instituto Gonçalo Moniz, Fundação Oswaldo Cruz (IGM/FIOCRUZ-BA), Salvador, Brazil.

The excessive release of heme during hemolysis contributes to the severity of sickle cell anemia (SCA) by exacerbating hemoglobin S (HbS) autoxidation, inflammation and systemic tissue damage. The present study investigated the effect of hydroxyurea (HU) on free radical neutralization and its stimulation of antioxidant genes in human peripheral blood mononuclear cells (PBMC) and human umbilical vein endothelial cells (HUVEC) in the presence or absence of hemin. HU (100 and 200 μM) significantly reduced the production of intracellular reactive oxygen species (ROS) induced by hemin at 70 μM in HUVEC. Read More

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AMPK Enhances Transcription of Selected Nrf2 Target Genes via Negative Regulation of Bach1.

Front Cell Dev Biol 2020 14;8:628. Epub 2020 Jul 14.

Department of Pharmacognosy, University of Vienna, Vienna, Austria.

5'-AMP-activated protein kinase (AMPK) and the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) are main players in the cellular adaptive response to metabolic and oxidative/xenobiotic stress, respectively. AMPK does not only balance the rate of fuel catabolism versus anabolism but also emerges as regulator of gene expression. We here examined the influence of AMPK on Nrf2-dependent gene transcription and the potential interplay of the two cellular stress hubs. Read More

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Oxidative Stress in Cancer.

Cancer Cell 2020 08 9;38(2):167-197. Epub 2020 Jul 9.

Department of Cell and Molecular Pharmacology, Medical University of South Carolina, Charleston, SC 29425, USA.

Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation, and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). Read More

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Evaluation of antioxidant capacity and immunomodulatory effects of yeast hydrolysates for hepatocytes of blunt snout bream (Megalobrama amblycephala).

Fish Shellfish Immunol 2020 Nov 12;106:142-148. Epub 2020 Jun 12.

National Experimental Teaching Demonstration Center of Animal Science, College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, PR China.

An in-vitro study was carried out to examine the effects of yeast hydrolysate (YH) on antioxidant capacity and innate immunity of blunt snout bream (Megalobrama amblycephala) hepatocytes. Fish primary hepatocytes were seeded at a density of 3 × 10 cells mL in 6-well tissue culture plates and treated with two different media including: 1) DMEM/F12 medium (control), and 2) YH medium [DMEM/F12 + 0.1 g L YH]. Read More

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November 2020

Treatment of dilated cardiomyopathy in a mouse model of Friedreich's ataxia using N-acetylcysteine and identification of alterations in microRNA expression that could be involved in its pathogenesis.

Pharmacol Res 2020 09 10;159:104994. Epub 2020 Jun 10.

Molecular Pharmacology and Pathology Program, Department of Pathology and Bosch Institute, Medical Foundation Building (K25), University of Sydney, Sydney, New South Wales, 2006 Australia; Centre for Cancer Cell Biology, Griffith Institute for Drug Discovery, Griffith University, Nathan, Brisbane, 4111, Queensland, Australia. Electronic address:

Deficient expression of the mitochondrial protein, frataxin, leads to a deadly cardiomyopathy. Our laboratory reported the master regulator of oxidative stress, nuclear factor erythroid 2-related factor-2 (Nrf2), demonstrates marked down-regulation after frataxin deletion in the heart. This was due, in part, to a pronounced increase in Keap1. Read More

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September 2020

In light-sensitive drug delivery system nanoparticles mediate oxidative stress.

Wei Xiang Long Chen

Am J Transl Res 2020 15;12(5):1469-1480. Epub 2020 May 15.

Bioengineering Institute of Chongqing University 174 Shazheng Street, Chongqing, China.

In light-sensitive drug delivery systems, more and more nanoparticles were applied to load various drug molecules. However, few studies focused on their biomedical effects such as the regulation of heme oxygenase-1 (HO-1) expression and reactive oxygen species (ROS) generation which could influence cellular redox reaction. In the present article, through review of literature, analysis of high-throughput sequencing database, the mechanisms of drug delivery based on organic (poly-lactic-co-glycolic acid (PLGA) and polyethylene glycol (PEG)) and inorganic (Au, ZnO, SiO and TiO) nanoparticles were introduced briefly. Read More

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Omega-3 fatty acids protect against acetaminophen-induced hepatic and renal toxicity in rats through HO-1-Nrf2-BACH1 pathway.

Arch Biochem Biophys 2020 07 26;687:108387. Epub 2020 Apr 26.

Department of Biochemistry, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.

Although acetaminophen (APAP) is a commonly used analgesic antipyretic drug, hepatotoxicity and nephrotoxicity are common after the overdose. The main mechanism of APAP toxicity is oxidative stress based. Stress may induce the production of heme oxygenase 1 (HO)-1 which is regulated by interleukin (IL)-10 and inhibit the production of tumor necrosis factor-alpha (TNF-α). Read More

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MicroRNA-based regulatory mechanisms underlying the synergistic antioxidant action of quercetin and catechin in HO-stimulated HepG2 cells: Roles of BACH1 in Nrf2-dependent pathways.

Free Radic Biol Med 2020 06 25;153:122-131. Epub 2020 Apr 25.

College of Food Science and Engineering, Shandong Agricultural University, Key Laboratory of Food Processing Technology and Quality Control of Shandong Higher Education Institutes, Taian, PR China. Electronic address:

The microRNA-based mechanisms underlying the antioxidant action(s) of co-existing flavonoids in response to oxidative stress are of high interest. This study aimed to extend the existing knowledge and provide insights into the potential regulatory network in response to oxidative stress and the co-presence of quercetin and catechin antioxidants, via a preclinical approach using HO-stimulated HepG2 cells. It was confirmed that BACH1 serves as an essential and direct negative regulator of the Keap1-Nrf2 signaling pathway and the antioxidant synergism between quercetin and catechin. Read More

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Transcription factors in ferroptotic cell death.

Cancer Gene Ther 2020 09 3;27(9):645-656. Epub 2020 Mar 3.

Department of Surgery, UT Southwestern Medical Center, Dallas, TX, 75390, USA.

Ferroptosis, a form of regulated cell death, is characterized by an excessive degree of iron accumulation and lipid peroxidation. Although it was originally identified only in cells expressing a mutant RAS oncogene, ferroptosis has also been found in normal cells following treatment by small molecules (e.g. Read More

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September 2020

Type I Interferon Response Dysregulates Host Iron Homeostasis and Enhances Candida glabrata Infection.

Cell Host Microbe 2020 Mar 18;27(3):454-466.e8. Epub 2020 Feb 18.

Medical University of Vienna, Center for Medical Biochemistry, Max Perutz Labs Vienna, Campus Vienna Biocenter, 1030 Vienna, Austria. Electronic address:

Type I interferons (IFNs-I) fulfil multiple protective functions during pathogenic infections, but they can also cause detrimental effects and enhance immunopathology. Here, we report that IFNs-I promote the dysregulation of iron homeostasis in macrophages during systemic infections with the intracellular pathogen Candida glabrata, leading to fungal survival and persistence. By engaging JAK1, IFNs-I disturb the balance of the transcriptional activator NRF2 and repressor BACH1 to induce downregulation of the key iron exporter Fpn1 in macrophages. Read More

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