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Article ; Online: The role of antipsychotics and other drugs on the development and progression of neuroleptic malignant syndrome.

Kyotani, Yoji / Zhao, Jing / Nakahira, Kiichi / Yoshizumi, Masanori

2023 Volume 13, Issue 1, Page(s) 18459

Abstract: Neuroleptic malignant syndrome (NMS) is a rare but serious and sometimes fatal complication in patients taking antipsychotic drugs, and its underlying mechanism still remains unclear. The pharmacotherapy for psychotic disorders is complicated and often ... ...

Abstract	Neuroleptic malignant syndrome (NMS) is a rare but serious and sometimes fatal complication in patients taking antipsychotic drugs, and its underlying mechanism still remains unclear. The pharmacotherapy for psychotic disorders is complicated and often involves a combination of two or more drugs, including drugs other than antipsychotics. In the present study, we used the Japanese Adverse Drug Event Report (JADER) database to broadly investigate the drugs associated with NMS, following their related pathways, as well as the drug-drug interactions (DDIs) in NMS. All analyses were performed using data from the JADER database from April 2004 to May 2022. Single-drug signals were evaluated using the reporting odds ratio (ROR) and proportional reporting ratio (PRR), and drug pathways were investigated using the Kyoto Encyclopedia of Genes and Genomes (KEGG). DDIs were evaluated using the Ω shrinkage measure and Chi-square statistics models. All drugs associated with 20 or more NMS cases in the JADER database exhibited signals for NMS, including non-antipsychotics. Pathways associated with the drugs included the dopaminergic or serotonergic synapses related to antipsychotics. DDIs leading to NMS were confirmed for several drug combinations exhibiting single-drug signals. This study confirmed the significant association of various drugs, including non-psychotics, with NMS and suggested that various pathways related to these drugs may be involved in the progression of NMS. In addition, several combinations of these drugs were found to interact (DDI), increasing the risk of NMS, which suggests that appropriate caution should be taken when administering these drugs.
MeSH term(s)	Humans ; Antipsychotic Agents/adverse effects ; Neuroleptic Malignant Syndrome/etiology ; Neuroleptic Malignant Syndrome/drug therapy ; Psychotic Disorders/drug therapy ; Drug-Related Side Effects and Adverse Reactions/complications ; Drug Interactions
Chemical Substances	Antipsychotic Agents
Language	English
Publishing date	2023-10-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-45783-z
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Article ; Online: Analysis of Appendicitis Cases in the Japanese Adverse Drug Event Report (JADER) Database.

Kyotani, Yoji / Zhao, Jing / Nakahira, Kiichi / Yoshizumi, Masanori

Biological & pharmaceutical bulletin

2023 Volume 46, Issue 5, Page(s) 655–660

Abstract: Appendicitis is one of the most common abdominal surgical emergencies worldwide; however, its causes remain poorly understood. The Japanese Adverse Drug Event Report (JADER) database is a spontaneous reporting system (SRS) that can be utilized to analyze ...

Abstract	Appendicitis is one of the most common abdominal surgical emergencies worldwide; however, its causes remain poorly understood. The Japanese Adverse Drug Event Report (JADER) database is a spontaneous reporting system (SRS) that can be utilized to analyze the safety signals of adverse events. In this study, we investigated the association between drug use and the onset of appendicitis using the JADER database. We first used the reporting odds ratio (ROR) as the signal and found signals for appendicitis, perforated appendicitis, and complicated appendicitis for 23, 9, and 1 drug, respectively. To investigate the level of hazard over time in drug-associated appendicitis, the Weibull shape parameter β was calculated using a Weibull plot, which revealed drug-dependent patterns for changes in the risk of appendicitis over time for the eight drugs. Furthermore, logistic regression analysis was performed to account for the influence of age, sex, and primary disease, and a significant association was detected between two drugs and appendicitis. Several types of drugs, such as antitumor, antirheumatic, and anti-inflammatory drugs, were included in our analyses; however, only clozapine, which is used for patients with schizophrenia, was commonly identified in these analyses. The resulting data suggest that certain drugs may be associated with appendicitis and may require adequate attention.
MeSH term(s)	Humans ; Adverse Drug Reaction Reporting Systems ; Appendicitis/epidemiology ; Databases, Factual ; Drug-Related Side Effects and Adverse Reactions/epidemiology ; Japan/epidemiology
Language	English
Publishing date	2023-04-30
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1150271-x
ISSN	1347-5215 ; 0918-6158
ISSN (online)	1347-5215
ISSN	0918-6158
DOI	10.1248/bpb.b22-00670
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Zs.A 1474: Show issues

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Article ; Online: Withdrawal: Carbon monoxide protects against hyperoxia-induced endothelial cell apoptosis by inhibiting reactive oxygen species formation.

Wang, Xue / Wang, Yong / Kim, Hong Pyo / Nakahira, Kiichi / Ryter, Stefan W / Choi, Augustine M K

The Journal of biological chemistry

2024 Volume 300, Issue 3, Page(s) 105758

Language	English
Publishing date	2024-02-19
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2024.105758
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Article: Targeting the mitogen-activated protein kinase-mediated vascular smooth muscle cell remodeling by angiotensin II.

Yoshizumi, Masanori / Kyotani, Yoji / Zhao, Jing / Nakahira, Kiichi

Annals of translational medicine

2020 Volume 8, Issue 5, Page(s) 157

Language	English
Publishing date	2020-03-18
Publishing country	China
Document type	Editorial ; Comment
ZDB-ID	2893931-1
ISSN	2305-5847 ; 2305-5839
ISSN (online)	2305-5847
ISSN	2305-5839
DOI	10.21037/atm.2019.12.145
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Article ; Online: Single cell profiling of γδ hepatosplenic T-cell lymphoma unravels tumor cell heterogeneity associated with disease progression.

Song, Wei / Zhang, Haixi / Yang, Fan / Nakahira, Kiichi / Wang, Cheng / Shi, Keqian / Zhang, Ruoyu

Cellular oncology (Dordrecht)

2022 Volume 46, Issue 1, Page(s) 211–226

Abstract: Purpose: Hepatosplenic T-cell lymphoma (HSTCL), mostly derived from γδ T cells, is a rare but very aggressive lymphoma with poor outcomes. In this study, we generated the first single cell landscape for this rare disease and characterized the molecular ... ...

Abstract	Purpose: Hepatosplenic T-cell lymphoma (HSTCL), mostly derived from γδ T cells, is a rare but very aggressive lymphoma with poor outcomes. In this study, we generated the first single cell landscape for this rare disease and characterized the molecular pathogenesis underlying the disease progression. Methods: We performed paired single cell RNA-seq and T cell receptor (TCR) sequencing on biopsies from a HSTCL patient pre- and post- chemotherapy treatments. Following by a series of bioinformatics analysis, we investigated the gene expression profile of γδ HSTCS as well as its tumor microenvironment (TME). Results: We characterized the unique gene expressing signatures of malignant γδ T cells with a set of marker genes were newly identified in HSTCL (AREG, PLEKHA5, VCAM1 etc.). Although the malignant γδ T cells were expanded from a single TCR clonotype, they evolved into two transcriptionally distinct tumor subtypes during the disease progression. The Tumor_1 subtype was dominant in pre-treatment samples with highly aggressive phenotypes. While the Tumor_2 had relative mild cancer hallmark signatures but expressed genes associated with tumor survival signal and drug resistance (IL32, TOX2, AIF1, AKAP12, CD38 etc.), and eventually became the main tumor subtype post-treatment. We further dissected the tumor microenvironment and discovered the dynamically rewiring cell-cell interaction networks during the treatment. The tumor cells had reduced communications with the microenvironment post-treatment. Conclusions: Our study reveals heterogenous and dynamic tumor and microenvironment underlying pathogenesis of HSTCL and may contribute to identify novel targets for diagnosis and treatment of HSTCL in the future.
MeSH term(s)	Humans ; Lymphoma, T-Cell/diagnosis ; Lymphoma, T-Cell/genetics ; Lymphoma, T-Cell/pathology ; Receptors, Antigen, T-Cell, gamma-delta/analysis ; Receptors, Antigen, T-Cell, gamma-delta/genetics ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Liver Neoplasms/metabolism ; Splenic Neoplasms/diagnosis ; Splenic Neoplasms/genetics ; Splenic Neoplasms/pathology ; Disease Progression ; Tumor Microenvironment
Chemical Substances	Receptors, Antigen, T-Cell, gamma-delta
Language	English
Publishing date	2022-11-22
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2595109-9
ISSN	2211-3436 ; 1875-8606 ; 2211-3428
ISSN (online)	2211-3436
ISSN	1875-8606 ; 2211-3428
DOI	10.1007/s13402-022-00745-x
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Zs.A 6908: Show issues

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Article ; Online: Retraction Notice to: mTORC1-Induced HK1-Dependent Glycolysis Regulates NLRP3 Inflammasome Activation.

Moon, Jong-Seok / Hisata, Shu / Park, Mi-Ae / DeNicola, Gina M / Ryter, Stefan W / Nakahira, Kiichi / Choi, Augustine M K

Cell reports

2023 Volume 42, Issue 6, Page(s) 112639

Language	English
Publishing date	2023-06-06
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.112639
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Article ; Online: Inflammasomes: Key Mediators of Lung Immunity.

Howrylak, Judie A / Nakahira, Kiichi

Annual review of physiology

2017 Volume 79, Page(s) 471–494

Abstract: Inflammasomes are key inflammatory signaling platforms that detect microbial substances, sterile environmental insults, and molecules derived from host cells. Activation of the inflammasome promotes caspase-1-mediated secretion of proinflammatory ... ...

Abstract	Inflammasomes are key inflammatory signaling platforms that detect microbial substances, sterile environmental insults, and molecules derived from host cells. Activation of the inflammasome promotes caspase-1-mediated secretion of proinflammatory cytokines interleukin (IL)-1β and IL-18 and pyroptosis. Recent developments in this field demonstrate the crucial role of the inflammasome in a wide range of disease models. Although inflammasomes are a crucial part of host defense mechanisms against pathogens, the exuberant immune response resulting from inflammasome activation also contributes to the development of various diseases. As ongoing studies further elucidate the regulation and function of the inflammasome, more evidence has emerged that the inflammasome appears to play a pivotal role in the development of multiple inflammatory diseases. Here, we discuss recent insights into how inflammasomes are regulated to activate caspase-1 and implicated in human diseases. We also review the contributions of the inflammasome to pulmonary diseases.
MeSH term(s)	Animals ; Caspase 1/metabolism ; Cytokines/metabolism ; Humans ; Immunity/immunology ; Inflammasomes/immunology ; Inflammasomes/metabolism ; Inflammation/immunology ; Inflammation/metabolism ; Lung/immunology ; Lung/metabolism ; Lung Diseases/immunology ; Lung Diseases/metabolism
Chemical Substances	Cytokines ; Inflammasomes ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2017--10
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	207933-1
ISSN	1545-1585 ; 0066-4278
ISSN (online)	1545-1585
ISSN	0066-4278
DOI	10.1146/annurev-physiol-021115-105229
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Article ; Online: Mitochondrial DNA Mutation, Diseases, and Nutrient-Regulated Mitophagy.

Yang, Xuan / Zhang, Ruoyu / Nakahira, Kiichi / Gu, Zhenglong

Annual review of nutrition

2019 Volume 39, Page(s) 201–226

Abstract: A wide spectrum of human diseases, including cancer, neurodegenerative diseases, and metabolic disorders, have been shown to be associated with mitochondrial dysfunction through multiple molecular mechanisms. Mitochondria are particularly susceptible to ... ...

Abstract	A wide spectrum of human diseases, including cancer, neurodegenerative diseases, and metabolic disorders, have been shown to be associated with mitochondrial dysfunction through multiple molecular mechanisms. Mitochondria are particularly susceptible to nutrient deficiencies, and nutritional intervention is an essential way to maintain mitochondrial homeostasis. Recent advances in genetic manipulation and next-generation sequencing reveal the crucial roles of mitochondrial DNA (mtDNA) in various pathophysiological conditions. Mitophagy, a term coined to describe autophagy that targets dysfunctional mitochondria, has emerged as an important cellular process to maintain mitochondrial homeostasis and has been shown to be regulated by various nutrients and nutritional stresses. Given the high prevalence of mtDNA mutations in humans and their impact on mitochondrial function, it is important to investigate the mechanisms that regulate mtDNA mutation. Here, we discuss mitochondrial genetics and mtDNA mutations and their implications for human diseases. We also examine the role of mitophagy as a therapeutic target, highlighting how nutrients may eliminate mtDNA mutations through mitophagy.
MeSH term(s)	DNA, Mitochondrial/genetics ; Gene Expression Regulation ; Humans ; Mitochondrial Diseases/genetics ; Mitophagy ; Nutrients
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2019-08-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	406980-8
ISSN	1545-4312 ; 0199-9885
ISSN (online)	1545-4312
ISSN	0199-9885
DOI	10.1146/annurev-nutr-082018-124643
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Zs.A 1786: Show issues

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Article ; Online: Upregulation of iNOS Protects Cyclic Mechanical Stretch-Induced Cell Death in Rat Aorta Smooth Muscle Cells.

Zhao, Jing / Nakahira, Kiichi / Kimura, Akihiko / Kyotani, Yoji / Yoshizumi, Masanori

International journal of molecular sciences

2020 Volume 21, Issue 22

Abstract: Aortic dissection and aneurysm are associated with abnormal hemodynamic loads originating from hypertension. Our previous study demonstrated that cyclic mechanical stretch (CMS, mimicked hypertension) caused the death of rat aortic smooth muscle cells ( ... ...

Abstract	Aortic dissection and aneurysm are associated with abnormal hemodynamic loads originating from hypertension. Our previous study demonstrated that cyclic mechanical stretch (CMS, mimicked hypertension) caused the death of rat aortic smooth muscle cells (RASMCs) in a mitogen activated-protein kinases (MAPKs)-dependent manner. The current study investigated the effects of inducible nitric oxide synthase (iNOS) on CMS-induced RASMC death. cDNA microarrays for CMS-treated RASMCs showed that iNOS expression levels were increased in response to CMS. Real-time polymerase chain reaction (PCR) analysis demonstrated that this increase was p38 MAPK (p38)-dependent. NO production was also increased. This increase could be inhibited by p38 and iNOS inhibitors. Thus, CMS-induced iNOS synthesized NO. CMS-induced cell death in RASMCs was increased by the iNOS inhibitor but abrogated by the long-acting NO donor DETA-NONOate. Increased iNOS expression was confirmed in the abdominal aortic constriction mouse model. Signal transducers and activators of transcription 1 (STAT1) was activated in stretched RASMCs, and iNOS expression and NO production were inhibited by the STAT1 inhibitor nifuroxazide. Our findings suggest that RASMCs were protected by iNOS from CMS-stimulated cell death through the STAT1 and p38 signal pathways independently.
MeSH term(s)	Animals ; Aorta/cytology ; Aorta/enzymology ; Gene Expression Regulation, Enzymologic ; Male ; Mechanotransduction, Cellular ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/enzymology ; Myocytes, Smooth Muscle/cytology ; Myocytes, Smooth Muscle/enzymology ; Nitric Oxide Synthase Type II/biosynthesis ; Rats ; Rats, Sprague-Dawley ; Stress, Mechanical ; Up-Regulation
Chemical Substances	Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, rat (EC 1.14.13.39)
Language	English
Publishing date	2020-11-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21228660
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Article ; Online: Conditional deletion of myeloid-specific mitofusin 2 but not mitofusin 1 promotes kidney fibrosis.

Bhatia, Divya / Capili, Allyson / Nakahira, Kiichi / Muthukumar, Thangamani / Torres, Lisa K / Choi, Augustine M K / Choi, Mary E

Kidney international

2022 Volume 101, Issue 5, Page(s) 963–986

Abstract: Macrophages exert critical functions during kidney injury, inflammation, and tissue repair or fibrosis. Mitochondrial structural and functional aberrations due to an imbalance in mitochondrial fusion/fission processes are implicated in the pathogenesis ... ...

Abstract	Macrophages exert critical functions during kidney injury, inflammation, and tissue repair or fibrosis. Mitochondrial structural and functional aberrations due to an imbalance in mitochondrial fusion/fission processes are implicated in the pathogenesis of chronic kidney disease. Therefore, we investigated macrophage-specific functions of mitochondrial fusion proteins, mitofusin (MFN)1 and MFN2, in modulating macrophage mitochondrial dynamics, biogenesis, oxidative stress, polarization, and fibrotic response. MFN1 and MFN2 were found to be suppressed in mice after adenine diet-induced chronic kidney disease, in transforming growth factor-beta 1-treated bone marrow-derived macrophages, and in THP-1-derived human macrophages (a human leukemic cell line). However, abrogating Mfn2 but not Mfn1 in myeloid-lineage cells resulted in greater macrophage recruitment into the kidney during fibrosis and the macrophage-derived fibrotic response associated with collagen deposition culminating in worsening kidney function. Myeloid-specific Mfn1 /Mfn2 double knockout mice also showed increased adenine-induced fibrosis. Mfn2-deficient bone marrow-derived macrophages displayed enhanced polarization towards the profibrotic/M2 phenotype and impaired mitochondrial biogenesis. Macrophages in the kidney of Mfn2-deficient and double knockout but not Mfn1-deficient mice exhibited greater mitochondrial mass, size, oxidative stress and lower mitophagy under fibrotic conditions than the macrophages in the kidney of wild-type mice. Thus, downregulation of MFN2 but not MFN1 lead to macrophage polarization towards a profibrotic phenotype to promote kidney fibrosis through a mechanism involving suppression of macrophage mitophagy and dysfunctional mitochondrial dynamics.
MeSH term(s)	Adenine/metabolism ; Animals ; Female ; Fibrosis ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Humans ; Kidney/pathology ; Male ; Mice ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Renal Insufficiency, Chronic/chemically induced ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/metabolism
Chemical Substances	Mitochondrial Proteins ; GTP Phosphohydrolases (EC 3.6.1.-) ; Adenine (JAC85A2161)
Language	English
Publishing date	2022-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2022.01.030
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Zs.A 797: Show issues

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