Iron is an essential trace metal element for maintaining vital functions, and it is involved in hemoglobin synthesis, redox reaction, enzyme activity, cell proliferation and apoptosis in various cells. Iron deficient-related diseases represented anemia are well-known, on the other hand, iron overload disease has attracted little attention. Excessive iron produces hydroxyl radicals via Fenton/Haber-Weiss reaction, causing organ damage in hereditary iron overload diseases. Additionally, it has been clarified that iron accumulation is involved in the pathological conditions even in metabolic diseases thought to be unrelated to iron so far. Therefore, the role of iron in the living body has been raised attention again. Recent studies have reported that body iron content is associated with both obesity and diabetes, and iron might be an aggravating factor of obesity and diabetes. We have revealed that iron chelating agent reduced oxidative stress and inflammation, suppressing the development of adipose hypertrophy in KKAy mice. Dietary iron restriction also diminishes oxidative stress, leading to the inhibition of increased albuminuria excretion and glomerular lesions in db/db mice. In this review, we give an outline of the role of iron on obese and diabetes, and diabetic kidney disease, and present the possibility of application to treatment with iron regulation in those disorders.
","ja":"鉄は生体内に最も多く存在する生命機能維持に必須の微量金属元素であり，赤血球のヘモグロビン合成，各種細胞における酸化還元反応，酵素活性，細胞増殖ならびにアポトーシスなどに関与する．そのため，貧血に代表される鉄欠乏疾患はよく知られているものの，鉄過剰疾患はあまり注目されてこなかった．過剰な鉄はフェントン/ハーバー・ワイス反応を介して酸化力が強力なヒドロキシルラジカルを生成し，遺伝性鉄過剰疾患における臓器障害の原因となるが，C型肝炎やアルツハイマー病などの従来は鉄と無関係と考えられていた疾患においても鉄が病態に関与していることが明らかとなり，生体内での鉄の役割が改めて注目されている．近年，生体内鉄量の増加が肥満ならびに糖尿病と関連することが示唆されており，鉄は肥満・糖尿病の増悪因子の可能性がある．しかし，肥満・糖尿病における鉄除去の効果については不明であった．我々は，肥満・糖尿病モデルKKAyマウスを用いて，鉄キレート剤投与が酸化ストレスや炎症を低減して，脂肪細胞肥大の進展が抑制されること，糖尿病性腎臓病モデルdb/dbマウスでは，食餌性鉄制限が酸化ストレスを減少して，アルブミン尿排泄増加や糸球体病変を抑制することで糖尿病性腎臓病の進行抑制につながることを報告した．本稿では，肥満・糖尿病とその合併症における鉄の役割と鉄制限による治療応用への可能性について，我々が明らかにした研究成果を含めて概説する．
"},"publication_date":"2019-12","publication_name":{"en":"Folia Pharmacologica Japonica","ja":"日本薬理学雑誌"},"volume":"Vol.154","number":"No.6","starting_page":"316","ending_page":"321","languages":["jpn"],"identifiers":{"doi":["10.1254/fpj.154.316"],"issn":["0015-5691"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:10, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://ci.nii.ac.jp/naid/120006464485/","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/111571","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050564288435540608/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=347857","label":"url"}],"paper_title":{"en":"The role of iron, a trace nutrient, on diabetes","ja":"糖尿病における微量栄養素「鉄」の役割"},"authors":{"en":[{"name":"Ikeda Yasumasa"}],"ja":[{"name":"池田 康将"}]},"description":{"en":"The nutrient balance is an important factor to keep healthy state in the body. In various nutrients, iron is a most abundant trace metal element. Iron-deficient anemia is often seen in the iron-related disorders, therefore, lots of functional food, drink, and nutritional supplement are widely provided and used to prevent iron deficiency. On the other hand, over iron intake induces excess iron status, causing increased oxidative stress production via catalyzing Fenton reaction. Recent evidences suggest that iron involves the pathological conditions of non-iron accumulating diseases, and the role of iron is noticed again.Diabetes is associated with poor prognosis to develop a variety of complications such as cardiovascular disease and diabetic kidney disease(DKD)in addition to diabetic retinopathy and neuropathy. Moreover, patients with diabetes often present reduced skeletal muscle mass, and it causes more impaired insulin resistance by diminishing glucose uptake. Recent studies have shown that iron content is associated with diabetic and obese condition, and high iron intake increases diabetes risk. We have clarified the favorable effect of iron reduction on obesity and DKD through diminishing oxidative stress. In addition, excess iron caused skeletal muscle atrophy and it was ameliorated by an anti-oxidant drug.Thus, iron plays an important role in diabetes and its complication through oxidative stress production. Further studies are clarifying an important role of trace nutrient including iron and so on, contributing to the development of new therapeutic strategy.","ja":"The nutrient balance is an important factor to keep healthy state in the body. In various nutrients, iron is a most abundant trace metal element. Iron-deficient anemia is often seen in the iron-related disorders, therefore, lots of functional food, drink, and nutritional supplement are widely provided and used to prevent iron deficiency. On the other hand, over iron intake induces excess iron status, causing increased oxidative stress production via catalyzing Fenton reaction. Recent evidences suggest that iron involves the pathological conditions of non-iron accumulating diseases, and the role of iron is noticed again.Diabetes is associated with poor prognosis to develop a variety of complications such as cardiovascular disease and diabetic kidney disease(DKD)in addition to diabetic retinopathy and neuropathy. Moreover, patients with diabetes often present reduced skeletal muscle mass, and it causes more impaired insulin resistance by diminishing glucose uptake. Recent studies have shown that iron content is associated with diabetic and obese condition, and high iron intake increases diabetes risk. We have clarified the favorable effect of iron reduction on obesity and DKD through diminishing oxidative stress. In addition, excess iron caused skeletal muscle atrophy and it was ameliorated by an anti-oxidant drug.Thus, iron plays an important role in diabetes and its complication through oxidative stress production. Further studies are clarifying an important role of trace nutrient including iron and so on, contributing to the development of new therapeutic strategy."},"publication_date":"2018-04-25","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.74","number":"No.1,2","starting_page":"13","ending_page":"20","languages":["jpn"],"identifiers":{"issn":["0037-3699"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:11, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/26522430","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84959258899&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=306912","label":"url"}],"paper_title":{"en":"Roles of the Androgen - Androgen Receptor System in Vascular Angiogenesis.","ja":"Roles of the Androgen - Androgen Receptor System in Vascular Angiogenesis."},"authors":{"en":[{"name":"Yoshida Sumiko"},{"name":"Ikeda Yasumasa"},{"name":"Aihara Ken-ichi"}],"ja":[{"name":"吉田 守美子"},{"name":"池田 康将"},{"name":"粟飯原 賢一"}]},"publication_date":"2016-03","publication_name":{"en":"Journal of Atherosclerosis and Thrombosis","ja":"Journal of Atherosclerosis and Thrombosis"},"volume":"Vol.23","number":"No.3","starting_page":"257","ending_page":"265","languages":["eng"],"identifiers":{"doi":["10.5551/jat.31047"],"issn":["1880-3873"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:12, {"insert":{"user_id":"B000241782","type":"misc","id":"30376242"},"force":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/24882646","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=278303","label":"url"}],"paper_title":{"en":"Drug development for cardiorenal disease based on oxidative stress control","ja":"酸化ストレス制御を基盤とする新規心腎血管障害治療薬の開発"},"authors":{"en":[{"name":"Imanishi Masaki"},{"name":"Ishizawa Keisuke"},{"name":"SAKURADA TAKUMI"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Yamano Noriko"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"今西 正樹"},{"name":"石澤 啓介"},{"name":"櫻田 巧"},{"name":"石澤 有紀"},{"name":"山野 範子"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"description":{"en":"Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review.","ja":"Oxidative stress is a key factor involved in the pathogenesis and progression of cardiovascular disease (CVD) and chronic kidney disease (CKD). Reactive oxygen species (ROS), produced as a result of redox reactions in various cells, have been recognized as key chemical mediators causing cellular damage and organ dysfunction in CVD and CKD. Nifedipine, a well-known calcium channel blocker, is extremely sensitive to light which gets converted to its nitroso analog, nitrosonifedipine (NO-NIF) in the presence of ultraviolet and visible light. The so formed NO-NIF blocks calcium channel quite weakly compared to that of nifedipine. However, we elucidated for the first time that NO-NIF is converted to NO-NIF radical which acquires extremely strong antioxidant property via reaction with unsaturated fatty acid or endothelial cells. We have already reported that NO-NIF reduces the cytotoxicity of cumene hydroperoxide, which hampers the integrity of cell membrane through oxidative stress, in endothelial cells. Additionally, we demonstrated that NO-NIF restored acetylcholine-responsive vascular relaxation and suppressed intercellular adhesion molecule-1 expression in the aorta of N(ω)-nitro-L-arginine methyl ester-treated rats, a model of vascular endothelial dysfunction. Recently, we reported that NO-NIF ameliorates angiotensin II-induced vascular remodeling via antioxidative effects in vivo and in vitro. These observations point towards the plausible, unique role of NO-NIF as a novel antioxidant which improves vascular dysfunction for overcoming CVD and CKD and the same has been highlighted in this review."},"publication_date":"2014-06","publication_name":{"en":"Journal of the Pharmaceutical Society of Japan","ja":"薬学雑誌"},"volume":"Vol.134","number":"No.6","starting_page":"715","ending_page":"719","languages":["jpn"],"identifiers":{"doi":["10.1248/yakushi.13-00255-4"],"issn":["1347-5231"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:13, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=277203","label":"url"}],"paper_title":{"en":"抗酸化薬","ja":"抗酸化薬"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2014-04-10","publication_name":{"en":"腎・高血圧の最新治療","ja":"腎・高血圧の最新治療"},"volume":"Vol.3","number":"No.2","starting_page":"93","ending_page":"99","languages":["jpn"],"invited":true,"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:14, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/40019952227/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1520290882774966784/","label":"url"},{"@id":"https://www.scopus.com/record/display.url?eid=2-s2.0-84892762387&origin=inward","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=274418","label":"url"}],"paper_title":{"en":"Role of Dietary Essential Trace Metals in the Pathogenesis of Diabetes Mellitus","ja":"糖尿病と食事由来金属元素"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2013-12","publication_name":{"en":"Journal of the The Japan Diabetes Society","ja":"糖尿病"},"volume":"Vol.56","number":"No.12","starting_page":"919","ending_page":"921","languages":["jpn"],"invited":true,"identifiers":{"issn":["0021-437X"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:15, {"insert":{"user_id":"B000241782","type":"misc","id":"30376244"},"force":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=313674","label":"url"}],"paper_title":{"en":"Nitrosonifedipineはangiotensin IIによるマウス血管リモデリングを抑制する","ja":"Nitrosonifedipineはangiotensin IIによるマウス血管リモデリングを抑制する"},"authors":{"en":[{"name":"櫻田 巧"},{"name":"Ishizawa Keisuke"},{"name":"Imanishi Masaki"},{"name":"藤井 聖子"},{"name":"谷口 順平"},{"name":"Izawa-Ishizawa Yuki"},{"name":"Miyamoto Licht"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tomita Shuhei"},{"name":"Minakuchi Kazuo"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"櫻田 巧"},{"name":"石澤 啓介"},{"name":"今西 正樹"},{"name":"藤井 聖子"},{"name":"谷口 順平"},{"name":"石澤 有紀"},{"name":"宮本 理人"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"冨田 修平"},{"name":"水口 和生"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2013-01-10","publication_name":{"en":"腎とフリーラジカル","ja":"腎とフリーラジカル"},"volume":"Vol.11","starting_page":"78","ending_page":"81","languages":["jpn"],"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:16, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22792467","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=253919","label":"url"}],"paper_title":{"en":"Effects of Statins on Cardiorenal Syndrome.","ja":"Effects of Statins on Cardiorenal Syndrome."},"authors":{"en":[{"name":"Yagi Shusuke"},{"name":"Aihara Ken-ichi"},{"name":"Ikeda Yasumasa"},{"name":"Akaike Masashi"},{"name":"Sata Masataka"},{"name":"Matsumoto Toshio"}],"ja":[{"name":"八木 秀介"},{"name":"粟飯原 賢一"},{"name":"池田 康将"},{"name":"赤池 雅史"},{"name":"佐田 政隆"},{"name":"松本 俊夫"}]},"description":{"en":"Cardiovascular disease and renal disease have a close relationship that forms a vicious cycle as a cardiorenal syndrome (CRS). Oxidative stress, endothelial dysfunction, and vascular inflammation could be therapeutic targets when the renin-angiotensin-aldosterone system is activated by accumulation of conventional cardiovascular risk factors; however, a strategy for management of CRS has not been established yet. Statins, HMG-CoA reductase inhibitors, have not only cholesterol-lowering effects but also pleiotropic effects on cardiovascular systems, including anti-inflammatory and antioxidant effects and improvement of nitric oxide bioavailability. Since recent studies have indicated that statins have beneficial effects on chronic kidney disease and heart failure as well as coronary artery disease in cholesterol-lowering-dependent/independent manners, treatment with statins might be a successful strategy for preventing deterioration of CRS.","ja":"Cardiovascular disease and renal disease have a close relationship that forms a vicious cycle as a cardiorenal syndrome (CRS). Oxidative stress, endothelial dysfunction, and vascular inflammation could be therapeutic targets when the renin-angiotensin-aldosterone system is activated by accumulation of conventional cardiovascular risk factors; however, a strategy for management of CRS has not been established yet. Statins, HMG-CoA reductase inhibitors, have not only cholesterol-lowering effects but also pleiotropic effects on cardiovascular systems, including anti-inflammatory and antioxidant effects and improvement of nitric oxide bioavailability. Since recent studies have indicated that statins have beneficial effects on chronic kidney disease and heart failure as well as coronary artery disease in cholesterol-lowering-dependent/independent manners, treatment with statins might be a successful strategy for preventing deterioration of CRS."},"publication_date":"2012-06-26","publication_name":{"en":"International Journal of Vascular Medicine","ja":"International Journal of Vascular Medicine"},"volume":"Vol.2012","starting_page":"162545","ending_page":"162545","languages":["eng"],"identifiers":{"doi":["10.1155/2012/162545"],"issn":["2090-2832"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:17, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=247531","label":"url"}],"paper_title":{"en":"Iron metabolism in the progression of adipocyte hypertrophy","ja":"Iron metabolism in the progression of adipocyte hypertrophy"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Tajima Soichiro"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"田島 壮一郎"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2012-06","publication_name":{"en":"The Cell","ja":"細胞"},"volume":"Vol.44","number":"No.6","starting_page":"282","ending_page":"286","languages":["jpn"],"invited":true,"identifiers":{"issn":["1346-7557"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:18, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/22493003","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=246743","label":"url"}],"paper_title":{"en":"Effects of androgens on cardiovascular remodeling.","ja":"Effects of androgens on cardiovascular remodeling."},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"Aihara Ken-ichi"},{"name":"Yoshida Sumiko"},{"name":"Akaike Masashi"},{"name":"Matsumoto Toshio"}],"ja":[{"name":"池田 康将"},{"name":"粟飯原 賢一"},{"name":"吉田 守美子"},{"name":"赤池 雅史"},{"name":"松本 俊夫"}]},"description":{"en":"Androgens, the male sex hormones, exert various biological effects on many target organs through the transcriptional effects of the nuclear androgen receptor (AR). ARs are expressed not only in classical target organs, such as the brain, genital organs, bone, and skeletal muscles, but also in the cardiovascular system. Because the female sex hormones estrogens are well known to protect against cardiovascular disease, sex has been considered to have a significant clinical impact on cardiovascular mortality. However, the influence of androgens on the cardiovascular system has not been fully elucidated. To clarify this issue, we analyzed the effects of administration of angiotensin II and doxorubicin, an anticancer agent, in a loading model in male wild-type and AR-deficient mice. In this review, we focus on the actions of androgens as potential targets for the prevention of cardiovascular diseases in males.","ja":"Androgens, the male sex hormones, exert various biological effects on many target organs through the transcriptional effects of the nuclear androgen receptor (AR). ARs are expressed not only in classical target organs, such as the brain, genital organs, bone, and skeletal muscles, but also in the cardiovascular system. Because the female sex hormones estrogens are well known to protect against cardiovascular disease, sex has been considered to have a significant clinical impact on cardiovascular mortality. However, the influence of androgens on the cardiovascular system has not been fully elucidated. To clarify this issue, we analyzed the effects of administration of angiotensin II and doxorubicin, an anticancer agent, in a loading model in male wild-type and AR-deficient mice. In this review, we focus on the actions of androgens as potential targets for the prevention of cardiovascular diseases in males."},"publication_date":"2012-04-05","publication_name":{"en":"The Journal of Endocrinology","ja":"The Journal of Endocrinology"},"languages":["eng"],"identifiers":{"doi":["10.1530/JOE-12-0126"],"issn":["1479-6805"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:19, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"http://ci.nii.ac.jp/naid/10029400903/","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1572543024868677632/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=231192","label":"url"}],"paper_title":{"en":"The role of iron on cardiovascular disease and diabetes mellitus","ja":"循環器疾患と糖尿病における生体内鉄の意義"},"authors":{"en":[{"name":"Ikeda Yasumasa"},{"name":"田島 壮一郎"},{"name":"Yamano Noriko"},{"name":"Tsuchiya Koichiro"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"池田 康将"},{"name":"田島 壮一郎"},{"name":"山野 範子"},{"name":"土屋 浩一郎"},{"name":"玉置 俊晃"}]},"publication_date":"2011-07-06","publication_name":{"en":"Japanese Journal of Circulation Research","ja":"血管"},"volume":"Vol.34","number":"No.2","starting_page":"75","ending_page":"85","languages":["jpn"],"identifiers":{"issn":["0911-4637"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:20, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"http://repo.lib.tokushima-u.ac.jp/110344","label":"url"},{"@id":"https://repo.lib.tokushima-u.ac.jp/ja/110344","label":"url"},{"@id":"https://cir.nii.ac.jp/crid/1050564287418524160/","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=230705","label":"url"}],"paper_title":{"en":"Role of Hypoxia-Inducible Factor1a (HIF-1a) in T cells in development of vascular remodeling","ja":"生体の低酸素応答と病態 -血管リモデリングにおける転写因子HIFの関与-"},"authors":{"en":[{"name":"Tomita Shuhei"},{"name":"Imanishi Masaki"},{"name":"Sakurada Takumi"},{"name":"Yamano Noriko"},{"name":"Kihira Yoshitaka"},{"name":"Ikeda Yasumasa"},{"name":"Tamaki Toshiaki"}],"ja":[{"name":"冨田 修平"},{"name":"今西 正樹"},{"name":"櫻田 巧"},{"name":"山野 範子"},{"name":"木平 孝高"},{"name":"池田 康将"},{"name":"玉置 俊晃"}]},"description":{"en":"Recent studies have shown that the cellular immune response to the hypoxic microenvironment constructed by vascular remodeling development modulates the resulting pathologic alterations. A major mechanism mediating adaptive responses to reduced oxygen availability is the regulation of transcription by hypoxia-inducible factor1(HIF‐1). Impairment of HIF‐1‐ dependent inflammatory responses in T cells causes an augmented vascular remodeling induced by arterial injury, which is shown as prominent neointimal hyperplasia and increase in infiltration of inflammatory cells at the adventitia in mice lacking Hif‐1α specifically in T cells. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice have shown enhanced production of cytokines in activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. This minireview shows that HIF‐1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of the T cell-mediated immune response and suggests potential new therapeutic strategies that target HIF‐1α.","ja":"Recent studies have shown that the cellular immune response to the hypoxic microenvironment constructed by vascular remodeling development modulates the resulting pathologic alterations. A major mechanism mediating adaptive responses to reduced oxygen availability is the regulation of transcription by hypoxia-inducible factor1(HIF‐1). Impairment of HIF‐1‐ dependent inflammatory responses in T cells causes an augmented vascular remodeling induced by arterial injury, which is shown as prominent neointimal hyperplasia and increase in infiltration of inflammatory cells at the adventitia in mice lacking Hif‐1α specifically in T cells. Studies to clarify the mechanism of augmented vascular remodeling in the mutant mice have shown enhanced production of cytokines in activated T cells and augmented antibody production in response to a T-dependent antigen in the mutant mice. This minireview shows that HIF‐1α in T cells plays a crucial role in vascular inflammation and remodeling in response to cuff injury as a negative regulator of the T cell-mediated immune response and suggests potential new therapeutic strategies that target HIF‐1α."},"publication_date":"2011-04-25","publication_name":{"en":"Shikoku Acta Medica","ja":"四国医学雑誌"},"volume":"Vol.67","number":"No.1, 2","starting_page":"3","ending_page":"6","languages":["jpn"],"identifiers":{"issn":["0037-3699"]},"misc_type":"introduction_scientific_journal"},"priority":"input_data"} line:21, {"insert":{"user_id":"B000241782","type":"misc"},"similar_merge":{"see_also":[{"@id":"https://www.ncbi.nlm.nih.gov/pubmed/21234356","label":"url"},{"@id":"https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=237315","label":"url"}],"paper_title":{"en":"Transforming Growth Factor-1 as a Common Target Molecule for Development of Cardiovascular Diseases, Renal Insufficiency and Metabolic Syndrome.","ja":"Transforming Growth Factor-1 as a Common Target Molecule for Development of Cardiovascular Diseases, Renal Insufficiency and Metabolic Syndrome."},"authors":{"en":[{"name":"Aihara Ken-ichi"},{"name":"Ikeda Yasumasa"},{"name":"Yagi Shusuke"},{"name":"Akaike Masashi"},{"name":"Matsumoto Toshio"}],"ja":[{"name":"粟飯原 賢一"},{"name":"池田 康将"},{"name":"八木 秀介"},{"name":"赤池 雅史"},{"name":"松本 俊夫"}]},"description":{"en":"Transforming growth factor-1 (TGF-1) is a polypeptide member of the transforming growth factor superfamily of cytokines. 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