Maho Tsubota 研究室

主宰者：Maho Tsubota

近畿大学

AI 要約（直近 5 年の研究成果）

Tsubota研究室は、化学療法や糖尿病に伴う末梢神経障害の発症メカニズムと治療法の開発に取り組んでいます。研究の中心となる問いは、がん治療薬や代謝疾患がなぜ神経傷害や疼痛を引き起こすのか、そしてそれをどのようにして予防・軽減できるかということです。具体的には、細胞核内タンパク質の細胞外への放出、特定のカルシウムチャネルの過剰活動、硫化水素などの生活活性分子の役割を解明することで、疾患の本態に迫っています。研究手法は、実験動物（主にマウスやラット）を用いた基礎研究と、医療機関や薬局の記録から得られた大規模臨床データの解析を組み合わせるという特徴を持ちます。in vivo実験では神経障害モデルを作製し、遺伝子改変や薬理学的介入により原因物質の役割を検証します。並行して、患者データベースを活用した観察研究を実施することで、基礎知見を臨床現場で検証しています。主な発見として、免疫細胞由来の核タンパク質の放出が複数の神経障害に共通して関与すること、T型カルシウムチャネルの活動を制御する微量元素や生理活性分子の重要性、既存医薬品がこれらの経路を標的として治療効果を発揮する可能性が報告されています。これらの成果は、既存薬の新たな治療応用や、より安全で効果的な治療戦略の開発につながる可能性があります。

※ AI（Claude）が、公開されている論文要旨から研究の問い・手法・主要な発見を事実情報として抽出・再構成して自動生成しています。誤りを含む可能性があるため、正確性は研究室公式情報でご確認ください。

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研究成果（34 件）

[2026] Involvement of Cav3.2 T-Type Ca2+ Channels and the Role of Endogenous Estrogen in Pruritus: Evidence from a Fundamental Study and Cross-Sectional Analysis of Pharmacy Claims Data
DOI: https://doi.org/10.1248/bpb.b25-00671
[2026] Chemotherapy-induced peripheral neuropathy and sex hormones
DOI: https://doi.org/10.1254/fpj.25102
[2025] HMGB1 derived from macrophages and enteric glial cells contributes to the butyrate-induced colonic hypersensitivity in mice
DOI: https://doi.org/10.1016/j.ejphar.2025.177660
[2025] Effectiveness of Angiotensin System Inhibitors Against Painful Peripheral Neuropathy in Type 2 Diabetic Old Patients: Validation by Analysis of Pharmacy Claims Data
DOI: https://doi.org/10.1248/yakushi.25-00083
[2025] Thrombomodulin-Induced Prevention of Peripheral Neuropathy in Oxaliplatin-Treated Mice Involves Complement C5a Inactivation and PAR1 Activation in Addition To HMGB1 Degradation
DOI: https://doi.org/10.1007/s11481-025-10262-x
[2025] HMGB1-Induced Neurite Outgrowth in the Dorsal Root Ganglion Neurons and Regeneration Priming after their Axonal Injury by Sciatic Nerve Crush
DOI: https://doi.org/10.1007/s11481-025-10261-y
[2024] Sulfide and polysulfide as pronociceptive mediators: Focus on Cav3.2 function enhancement and TRPA1 activation
DOI: https://doi.org/10.1016/j.jphs.2024.04.007
[2024] Involvement of Cav3.2 T-type Ca2+ channels and cystathionine-β-synthase in colitis-related visceral hypersensitivity in mice
DOI: https://doi.org/10.1016/j.jphs.2024.09.003
[2024] Clinical and preclinical evidence that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers prevent diabetic peripheral neuropathy
DOI: https://doi.org/10.1038/s41598-024-51572-z
[2023] Dietary Zinc Deficiency Induces Cav3.2-Dependent Nociceptive Hypersensitivity in Mice
DOI: https://doi.org/10.1248/bpb.b23-00270

続きを表示（残り 24 件）

[2023] Cav3.2-dependent hyperalgesia/allodynia following intrathecal and intraplantar zinc chelator administration in rodents
DOI: https://doi.org/10.1016/j.jphs.2023.03.007
[2023] Carbidopa and benserazide that inhibit cystathionine-β-synthase, an H2S-forming enzyme, suppress the viability of both bortezomib-sensitive and -resistant multiple myeloma cells
DOI: https://doi.org/10.1254/jpssuppl.97.0_3-b-o14-2
[2023] Role of HMGB1 and anaphylatoxin C5a in the development of painful peripheral neuropathy in leptin receptor-deficient db/db mice and high fat diet-fed type 2 diabetic mice
DOI: https://doi.org/10.1254/jpssuppl.97.0_2-b-ss07-2
[2023] KTtp38, a novel pimozide derivative, suppresses T-type calcium channel-dependent somatic and visceral pain
DOI: https://doi.org/10.1254/jpssuppl.97.0_2-b-ss07-1
[2023] Identification of cells that release HMGB1 responsible for colonic hypersensitivity in a mouse model for irritable bowel syndrome and its prevention by azeliragon, a RAGE antagonist, and sulfasalazine, an anti-arthritis/anti-colitis medicine
DOI: https://doi.org/10.1254/jpssuppl.97.0_3-b-p-015
[2022] Discovery of pimozide derivatives as novel T-type calcium channel inhibitors with little binding affinity to dopamine D2 receptors for treatment of somatic and visceral pain
DOI: https://doi.org/10.1016/j.ejmech.2022.114716
[2022] A hydrolysate of poly-trans-[(2-carboxyethyl)germasesquioxane] (Ge-132) suppresses Cav3.2-dependent pain by sequestering exogenous and endogenous sulfide
DOI: https://doi.org/10.1016/j.redox.2022.102579
[2022] Opioid modulation of T-type Ca2+ channel-dependent neuritogenesis/neurite outgrowth through the prostaglandin E2/EP4 receptor/protein kinase A pathway in mouse dorsal root ganglion neurons
DOI: https://doi.org/10.1016/j.bbrc.2022.11.108
[2022] Development of hepatic impairment aggravates chemotherapy-induced peripheral neuropathy following oxaliplatin treatment: Evidence from clinical and preclinical studies
DOI: https://doi.org/10.1016/j.jphs.2022.01.006
[2022] Inhibition of endogenous H2S production suppresses the viability of multiple myeloma cells: application of carbidopa and benserazide capable of inhibiting cystathionine-β-synthase to treatment of bortezomib-resistant multiple myeloma
DOI: https://doi.org/10.1254/jpssuppl.95.0_3-p-266
[2022] Sulfasalazine, an anti-rheumatic agent, relieves inflammatory pain by reducing Toll-like receptor 4-mediated HMGB1 release from macrophages
DOI: https://doi.org/10.1254/jpssuppl.95.0_2-yia-40
[2022] Diabetic peripheral neuropathy is inhibited by thrombomodulin alfa in a thrombin-dependent manner and aggravated by anticoagulants: novel evidence from integration of preclinical and clinical studies
DOI: https://doi.org/10.1254/jpssuppl.95.0_2-yia-55
[2022] TAFIa/carboxypeptidase B generated by the thrombomodulin/thrombin system prevents oxaliplatin-induced peripheral neuropathy through inactivation of complement component C5a
DOI: https://doi.org/10.1254/jpssuppl.95.0_1-ss-30
[2022] Activated protein C suppresses neuropathic pain through activation of proteinase-activated receptor 1 (PAR1)
DOI: https://doi.org/10.1254/jpssuppl.96.0_1-b-ss08-3
[2022] A novel T-type Ca2+ channel inhibitor, KTtp38, developed by structural modifications of pimozide, a typical antipsychotic agent: Evaluation of the channel selectivity, electrophysiological characteristics and analgesic activity
DOI: https://doi.org/10.1254/jpssuppl.96.0_1-b-ss06-6
[2022] Involvement of platelet-derived HMGB1 in oxaliplatin-induced peripheral neuropathy (OIPN): OIPN prevention by antiplatelet agents
DOI: https://doi.org/10.1254/jpssuppl.96.0_2-b-o04-4
[2021] Role of neuron-derived ATP in paclitaxel-induced HMGB1 release from macrophages and peripheral neuropathy
DOI: https://doi.org/10.1016/j.jphs.2021.11.003
[2021] Caspase-Dependent HMGB1 Release from Macrophages Participates in Peripheral Neuropathy Caused by Bortezomib, a Proteasome-Inhibiting Chemotherapeutic Agent, in Mice
DOI: https://doi.org/10.3390/cells10102550
[2021] Estrogen decline is a risk factor for paclitaxel-induced peripheral neuropathy: Clinical evidence supported by a preclinical study
DOI: https://doi.org/10.1016/j.jphs.2021.03.001
[2021] Effects of Bepridil and Pimozide, Existing Medicines Capable of Blocking T-Type Ca2+ Channels, on Visceral Pain in Mice
DOI: https://doi.org/10.1248/bpb.b20-00742
[2021] A thrombin inhibitor aggravates HMGB1-dependent colonic and bladder pain: Role of the thrombomodulin/thrombin system in visceral pain modulation
DOI: https://doi.org/10.1254/jpssuppl.94.0_1-o-b2-2
[2021] Macrophage-derived HMGB1 contributes to the accelerated neurite outgrowth in dorsal root ganglion neurons isolated from the mice subjected to sciatic nerve injury
DOI: https://doi.org/10.1254/jpssuppl.94.0_2-p1-26
[2021] Exacerbation of paclitaxel-induced peripheral neuropathy and HMGB1-induced allodynia in ovariectomized mice
DOI: https://doi.org/10.1254/jpssuppl.94.0_1-o-b2-3
[2021] Itch and pain caused by intradermal injection of sulfides in mouse cheek: Effect of genetic deletion of Cav3.2 T-type calcium channels
DOI: https://doi.org/10.1254/jpssuppl.94.0_3-p1-08

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AI 要約（直近 5 年の研究成果）

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研究成果（34 件）

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