Details of a Researcher - FURUHASHI Masato

Papers - FURUHASHI Masato

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家族性高コレステロール血症における残余リスクマーカーとしての脂肪酸結合蛋白

小倉正恒, 古橋眞人, 森本めぐむ, 松本めぐみ, 三浦哲嗣, 斯波真理子

日本動脈硬化学会総会プログラム・抄録集 ( (一社)日本動脈硬化学会 ) 48回 201 - 201 2016.06

Local Production of Fatty Acid-Binding Protein 4 in Epicardial/Perivascular Fat and Macrophages Is Linked to Coronary Atherosclerosis

Masato Furuhashi, Takahiro Fuseya, Masaki Murata, Kyoko Hoshina, Shutaro Ishimura, Tomohiro Mita, Yuki Watanabe, Akina Omori, Megumi Matsumoto, Takeshi Sugaya, Tsuyoshi Oikawa, Junichi Nishida, Nobuaki Kokubu, Marenao Tanaka, Norihito Moniwa, Hideaki Yoshida, Norimasa Sawada, Kazuaki Shimamoto, Tetsuji Miura

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY ( LIPPINCOTT WILLIAMS & WILKINS ) 36 ( 5 ) 825 - 834 2016.05 [Refereed]

Objective-Fatty acid-binding protein 4 (FABP4) is expressed in adipocytes and macrophages, and elevated circulating FABP4 level is associated with obesity-mediated metabolic phenotype. We systematically investigated roles of FABP4 in the development of coronary artery atherosclerosis. Approach and Results-First, by immunohistochemical analyses, we found that FABP4 was expressed in macrophages within coronary atherosclerotic plaques and epicardial/perivascular fat in autopsy cases and macrophages within thrombi covering ruptured coronary plaques in thrombectomy samples from patients with acute myocardial infarction. Second, we confirmed that FABP4 was secreted from macrophages and adipocytes cultured in vitro. Third, we investigated the effect of exogenous FABP4 on macrophages and human coronary artery-derived smooth muscle cells and endothelial cells in vitro. Treatment of the cells with recombinant FABP4 significantly increased gene expression of inflammatory markers in a dose-dependent manner. Finally, we measured serum FABP4 level in the aortic root (Ao-FABP4) and coronary sinus (CS-FABP4) of 34 patients with suspected or known coronary artery disease. Coronary stenosis score assessed by the modified Gensini score was weakly correlated with CS-FABP4 but was not correlated with Ao-FABP4. A stronger correlation (r=0.59, P<0.01) was observed for the relationship between coronary stenosis score and coronary veno-arterial difference in FABP4 level, (CS-Ao)-FABP4, indicating local production of FABP4 during coronary circulation in the heart. Multivariate analysis indicated that (CS-Ao)-FABP4 was an independent predictor of the severity of coronary stenosis after adjustment of conventional risk factors. Conclusions-FABP4 locally produced by epicardial/perivascular fat and macrophages in vascular plaques contributes to the development of coronary atherosclerosis.

DOI

植込み型除細動器導入症例におけるCKDの臨床的特徴

茂庭仁人, 瀬野結, 田中希尚, 古橋眞人, 吉田英昭, 藤戸健史, 望月敦史, 永原大五, 三浦哲嗣

日本腎臓学会誌 ( (一社)日本腎臓学会 ) 58 ( 3 ) 280 - 280 2016.05

当院における植込み型除細動器導入透析患者の特徴

茂庭仁人, 瀬野結, 田中希尚, 古橋眞人, 吉田英昭, 藤戸健史, 望月敦史, 永原大五, 三浦哲嗣

日本透析医学会雑誌 ( (一社)日本透析医学会 ) 49 ( Suppl.1 ) 799 - 799 2016.05

Possible Increase in Serum FABP4 Level Despite Adiposity Reduction by Canagliflozin, an SGLT2 Inhibitor

Masato Furuhashi, Megumi Matsumoto, Shinya Hiramitsu, Akina Omori, Marenao Tanaka, Norihito Moniwa, Hideaki Yoshida, Junnichi Ishii, Tetsuji Miura

PLOS ONE ( PUBLIC LIBRARY SCIENCE ) 11 ( 4 ) 2016.04 [Refereed]

Background Fatty acid-binding protein 4 (FABP4/A-FABP/aP2) is secreted from adipocytes in association with catecholamine-induced lipolysis, and elevated serum FABP4 level is associated with obesity, insulin resistance and atherosclerosis. Secreted FABP4 as a novel adipokine leads to insulin resistance via increased hepatic glucose production (HGP). Sodium-glucose cotransporter 2 (SGLT2) inhibitors decrease blood glucose level via increased urinary glucose excretion, though HGP is enhanced. Here we investigated whether canagliflozin, an SGLT2 inhibitor, modulates serum FABP4 level. Methods Canagliflozin (100 mg/day) was administered to type 2 diabetic patients (n = 39) for 12 weeks. Serum FABP4 level was measured before and after treatment. Results At baseline, serum FABP4 level was correlated with adiposity, renal dysfunction and noradrenaline level. Treatment with canagliflozin significantly decreased adiposity and levels of fasting glucose and HbA1c but increased average serum FABP4 level by 10.3%(18.0 +/- 1.0 vs. 19.8 +/- 1.2 ng/ml, P = 0.008), though elevation of FABP4 level after treatment was observed in 26 (66.7%) out of 39 patients. Change in FABP4 level was positively correlated with change in levels of fasting glucose (r = 0.329, P = 0.044), HbA1c (r = 0.329, P = 0.044) and noradrenaline (r = 0.329, P = 0.041) but was not significantly correlated with change in adiposity or other variables. Conclusions Canagliflozin paradoxically increases serum FABP4 level in some diabetic patients despite amelioration of glucose metabolism and adiposity reduction, possibly via induction of catecholamine-induced lipolysis in adipocytes. Increased FABP4 level by canagliflozin may undermine the improvement of glucose metabolism and might be a possible mechanism of increased HGP by inhibition of SGLT2.

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SGLT2阻害薬であるカナグリフロジンによる新規アディポカイン脂肪酸結合タンパク4(FABP4)の血中濃度への影響

古橋眞人, 松本めぐみ, 平光伸也, 大森晶奈, 田中希尚, 茂庭仁人, 吉田英昭, 石井潤一, 三浦哲嗣

糖尿病 ( (一社)日本糖尿病学会 ) 59 ( Suppl.1 ) S - 336 2016.04

睡眠呼吸障害が血糖変動に与える影響の検討

中田圭, 丹野雅也, 矢野俊之, 小笠原淳, 赤坂憲, 古橋眞人, 三木隆幸, 三浦哲嗣

糖尿病 ( (一社)日本糖尿病学会 ) 59 ( Suppl.1 ) S - 191 2016.04

Reduction of circulating FABP4 level by treatment with omega-3 fatty acid ethyl esters

Masato Furuhashi, Shinya Hiramitsu, Tomohiro Mita, Akina Omori, Takahiro Fuseya, Shutaro Ishimura, Yuki Watanabe, Kyoko Hoshina, Megumi Matsumoto, Marenao Tanaka, Norihito Moniwa, Hideaki Yoshida, Junnichi Ishii, Tetsuji Miura

LIPIDS IN HEALTH AND DISEASE ( BIOMED CENTRAL LTD ) 15 2016.01 [Refereed]

Background: Fatty acid-binding protein 4 (FABP4/A-FABP/aP2) mainly expressed in adipocytes is secreted and acts as an adipokine. Increased circulating FABP4 level is associated with obesity, insulin resistance and atherosclerosis. However, little is known about the modulation of serum FABP4 level by drugs including anti-dyslipidemic agents. Methods: Patients with dyslipidemia were treated with omega-3 fatty acid ethyl esters (4 g/day; n = 14) containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) for 4 weeks. Serum FABP4 level was measured before and after treatment. Expression and secretion of FABP4 were also examined in mouse 3T3-L1 adipocytes treated with EPA or DHA. Results: Treatment with omega-3 fatty acid ethyl esters significantly decreased triglycerides and serum FABP4 level (13.5 +/- 1.5 vs. 11.5 +/- 1.1 ng/ml, P = 0.017). Change in FABP4 level by omega-3 fatty acids was negatively correlated with change in levels of EPA + DHA (r = -0.643, P = 0.013), EPA (r = -0.540, P = 0.046) and DHA (r = -0.650, P = 0.011) but not change in the level of triglycerides or other fatty acid composition. Treatment of 3T3-L1 adipocytes with EPA or DHA had no effect on short-term (2 h) secretion of FABP4. However, gene expression and long-term (24 h) secretion of FABP4 were significantly reduced by treatment with EPA or DHA. Conclusions: Omega-3 fatty acids decrease circulating FABP4 level, possibly by reducing expression and consecutive secretion of FABP4 in adipocytes. Reducing FABP4 level might be involved in suppression of cardiovascular events by omega-3 fatty acids.

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Reduction of serum FABP4 level by sitagliptin, a DPP-4 inhibitor, in patients with type 2 diabetes mellitus

Masato Furuhashi, Shinya Hiramitsu, Tomohiro Mita, Takahiro Fuseya, Shutaro Ishimura, Akina Omori, Megumi Matsumoto, Yuki Watanabe, Kyoko Hoshina, Marenao Tanaka, Norihito Moniwa, Hideaki Yoshida, Junnichi Ishii, Tetsuji Miura

JOURNAL OF LIPID RESEARCH ( AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC ) 56 ( 12 ) 2372 - 2380 2015.12 [Refereed]

Fatty acid binding protein 4 (FABP4), also known as adipocyte FABP or aP2, is secreted from adipocytes in association with lipolysis as a novel adipokine, and elevated serum FABP4 level is associated with obesity, insulin resistance, and atherosclerosis. However, little is known about the modulation of serum FABP4 level by therapeutic drugs. Sitagliptin (50 mg/day), a dipeptidyl peptidase 4 (DPP-4) inhibitor that increases glucagon-like peptide 1 (GLP-1), was administered to patients with type 2 diabetes (n = 24) for 12 weeks. Treatment with sitagliptin decreased serum FABP4 concentration by 19.7% (17.8 +/- 1.8 vs. 14.3 +/- 1.5 ng/ml, P < 0.001) and hemoglobin A1c without significant changes in adiposity or lipid variables. In 3T3-L1 adipocytes, sitagliptin or exendin-4, a GLP-1 receptor agonist, had no effect on short-term (2 h) secretion of FABP4. However, gene expression and long-term (24 h) secretion of FABP4 were significantly reduced by sitagliptin, which was not mimicked by exendin-4. Treatment with recombinant DPP-4 increased gene expression and long-term secretion of FABP4, and the effects were cancelled by sitagliptin. Furthermore, knockdown of DPP-4 in 3T3-L1 adipocytes decreased gene expression and long-term secretion of FABP4. In conclusion, sitagliptin decreases serum FABP4 level, at least in part, via reduction in the expression and consecutive secretion of FABP4 in adipocytes by direct inhibition of DPP-4.

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シタグリプチンは新規アディポカイン脂肪酸結合タンパク4(FABP4)の血中濃度を低下させる

古橋眞人, 平光伸也, 石井潤一, 美田知宏, 大森晶奈, 伏屋敬博, 石村周太郎, 渡邊礼, 松本めぐみ, 田中希尚, 茂庭仁人, 吉田英昭, 三浦哲嗣

肥満研究 ( (一社)日本肥満学会 ) 21 ( Suppl. ) 175 - 175 2015.09

Angiotensin II receptor blockers decrease serum concentration of fatty acid-binding protein 4 in patients with hypertension

Masato Furuhashi, Tomohiro Mita, Norihito Moniwa, Kyoko Hoshina, Shutaro Ishimura, Takahiro Fuseya, Yuki Watanabe, Hideaki Yoshida, Kazuaki Shimamoto, Tetsuji Miura

HYPERTENSION RESEARCH ( NATURE PUBLISHING GROUP ) 38 ( 4 ) 252 - 259 2015.04 [Refereed]

Elevated circulating fatty acid-binding protein 4 (FABP4/A-FABP/aP2), an adipokine, is associated with obesity, insulin resistance, hypertension and cardiovascular events. However, how circulating FABP4 level is modified by pharmacological agents remains unclear. We here examined the effects of angiotensin II receptor blockers (ARBs) on serum FABP4 level. First, essential hypertensives were treated with ARBs: candesartan (8 mg day-1; n= 7) for 2 weeks, olmesartan (20 mg day-1; n= 9) for 12 weeks, and valsartan (80 mg day-1; n= 94) or telmisartan (40 mg day-1; n= 91) for 8 weeks added to amlodipine (5 mg day-1). Treatment with ARBs significantly decreased blood pressure and serum FABP4 concentrations by 8-20% without significant changes in adiposity or lipid variables, though the M value determined by hyperinsulinemic-euglycemic glucose clamp, a sensitive index of insulin sensitivity, was significantly increased by candesartan. Next, alterations in FABP4 secretion from 3T3-L1 adipocytes were examined under several agents. Lipolytic stimulation of the beta-adrenoceptor in 3T3-L1 adipocytes by isoproterenol increased FABP4 secretion, and conversely, insulin suppressed FABP4 secretion. However, treatment of 3T3-L1 adipocytes with angiotensin II or ARBs for 2 h had no effect on gene expression or secretion of FABP4 regardless of beta-adrenoceptor stimulation. In conclusion, treatment with structurally different ARBs similarly decreases circulating FABP4 concentrations in hypertensive patients as a class effect of ARBs, which is not attributable to blockade of the angiotensin II receptor in adipocytes. Reduction of FABP4 levels by ARBs might be involved in suppression of cardiovascular events.

DOI PubMed

オメガ-3脂肪酸エチルは新規アディポカイン脂肪酸結合タンパク4の血中濃度を低下させる

古橋眞人, 平光伸也, 石井潤一, 美田知宏, 大森晶奈, 伏屋敬博, 石村周太郎, 渡邊礼, 田中希尚, 吉田英昭, 三浦哲嗣

糖尿病 ( (一社)日本糖尿病学会 ) 58 ( Suppl.1 ) S - 146 2015.04

FABP4 is Secreted from Adipocytes by Adenyl Cyclase-PKA- and Guanylyl Cyclase-PKG-Dependent Lipolytic Mechanisms

Tomohiro Mita, Masato Furuhashi, Shinya Hiramitsu, Junnichi Ishii, Kyoko Hoshina, Shutaro Ishimura, Takahiro Fuseya, Yuki Watanabe, Marenao Tanaka, Kohei Ohno, Hiroshi Akasaka, Hirofumi Ohnishi, Hideaki Yoshida, Shigeyuki Saitoh, Kazuaki Shimamoto, Tetsuji Miura

OBESITY ( WILEY-BLACKWELL ) 23 ( 2 ) 359 - 367 2015.02 [Refereed]

ObjectiveFatty acid-binding protein 4 (FABP4) is expressed in adipocytes, and elevated plasma FABP4 level is associated with obesity-mediated metabolic phenotype. Postprandial regulation and secretory signaling of FABP4 has been investigated. MethodsTime courses of FABP4 levels were examined during an oral glucose tolerance test (OGTT; n=53) or a high-fat test meal eating (n=35). Effects of activators and inhibitors of adenyl cyclase (AC)-protein kinase A (PKA) signaling and guanylyl cyclase (GC)-protein kinase G (PKG) signaling on FABP4 secretion from mouse 3T3-L1 adipocytes were investigated. ResultsFABP4 level significantly declined after the OGTT or a high-fat meal eating, while insulin level was increased. Treatment with low and high glucose concentration or palmitate for 2 h did not affect FABP4 secretion from 3T3-L1 adipocytes. FABP4 secretion was increased by stimulation of lipolysis using isoproterenol, a (3)-adrenoceptor agonist (CL316243), forskolin, dibutyryl-cAMP and atrial natriuretic peptide, and the induced FABP4 secretion was suppressed by insulin or an inhibitor of PKA (H-89), PKG (KT5823) or hormone sensitive lipase (CAY10499). ConclusionsFABP4 is secreted from adipocytes in association with lipolysis regulated by AC-PKA- and GC-PKG-mediated signal pathways. Plasma FABP4 level declines postprandially, and suppression of FABP4 secretion by insulin-induced anti-lipolytic signaling may be involved in this decline in FABP4 level.

DOI PubMed

Urinary Angiotensin-Converting Enzyme 2 in Hypertensive Patients May Be Increased by Olmesartan, an Angiotensin II Receptor Blocker

Masato Furuhashi, Norihito Moniwa, Tomohiro Mita, Takahiro Fuseya, Shutaro Ishimura, Kohei Ohno, Satoru Shibata, Marenao Tanaka, Yuki Watanabe, Hiroshi Akasaka, Hirofumi Ohnishi, Hideaki Yoshida, Hideki Takizawa, Shigeyuki Saitoh, Nobuyuki Ura, Kazuaki Shimamoto, Tetsuji Miura

AMERICAN JOURNAL OF HYPERTENSION ( OXFORD UNIV PRESS ) 28 ( 1 ) 15 - 21 2015.01 [Refereed]

BACKGROUND Angiotensin-converting enzyme 2 (ACE2) is highly expressed in the kidney and converts angiotensin (Ang) II to Ang-(1-7), a renoprotective peptide. Urinary ACE2 has been shown to be elevated in patients with chronic kidney disease. However, the effects of antihypertensive agents on urinary ACE2 remain unclear. METHODS Of participants in the Tanno-Sobetsu cohort study in 2011 (n = 617), subjects on no medication (n = 101) and hypertensive patients treated with antihypertensive agents, including the calcium channel blockers amlodipine and long-acting nifedipine; the ACE inhibitor enalapril; and the Ang II receptor blockers losartan, candesartan, valsartan, telmisartan, and olmesartan, for more than 1 year (n = 100) were enrolled, and urinary ACE2 level was measured. RESULTS Glucose and hemoglobin A1c were significantly higher in patients treated with enalapril, telmisartan or olmesartan than in the control subjects. Urinary albumin-to-creatinine ratio (UACR) was significantly higher in patients treated with enalapril than in the control subjects. Urinary ACE2 level was higher in the olmesartan-treated group, but not the other treatment groups, than in the control group. Urinary ACE2 level was positively correlated with systolic blood pressure (r = 0.211; P = 0.003), UACR (r = 0.367; P < 0.001), and estimated salt intake (r = 0.260; P < 0.001). Multivariable regression analysis after adjustment of age, sex, and the correlated indices showed that the use of olmesartan was an independent predictor of urinary ACE2 level. CONCLUSIONS In contrast with other antihypertensive drugs, olmesartan may uniquely increase urinary ACE2 level, which could potentially offer additional renoprotective effects.

DOI PubMed

Fatty acid-binding protein 4 (FABP4): Pathophysiological insights and potent clinical biomarker of metabolic and cardiovascular diseases

Masato Furuhashi, Shigeyuki Saitoh, Kazuaki Shimamoto, Tetsuji Miura

Clinical Medicine Insights: Cardiology ( Libertas Academica Ltd. ) 2014 23 - 33 2014.12 [Refereed]

Over the past decade, evidences of an integration of metabolic and inflammatory pathways, referred to as metaflammation in several aspects of metabolic syndrome, have been accumulating. Fatty acid-binding protein 4 (FABP4), also known as adipocyte FABP (A-FABP) or aP2, is mainly expressed in adipocytes and macrophages and plays an important role in the development of insulin resistance and atherosclerosis in relation to metaflam-mation. Despite lack of a typical secretory signal peptide, FABP4 has been shown to be released from adipocytes in a non-classical pathway associated with lipolysis, possibly acting as an adipokine. Elevation of circulating FABP4 levels is associated with obesity, insulin resistance, diabetes mellitus, hyperten-sion, cardiac dysfunction, atherosclerosis, and cardiovascular events. Furthermore, ectopic expression and function of FABP4 in several types of cells and tissues have been recently demonstrated. Here, we discuss both the significant role of FABP4 in pathophysiological insights and its usefulness as a biomarker of metabolic and cardiovascular diseases.

DOI PubMed

Urinary Excretion of Fatty Acid-Binding Protein 4 is Associated with Albuminuria and Renal Dysfunction

Yusuke Okazaki, Masato Furuhashi, Marenao Tanaka, Tomohiro Mita, Takahiro Fuseya, Shutaro Ishimura, Yuki Watanabe, Kyoko Hoshina, Hiroshi Akasaka, Hirofumi Ohnishi, Hideaki Yoshida, Shigeyuki Saitoh, Kazuaki Shimamoto, Tetsuji Miura

PLOS ONE ( PUBLIC LIBRARY SCIENCE ) 9 ( 12 ) e115429 2014.12 [Refereed]

Background: Fatty acid-binding protein 4 (FABP4/A-FABP/aP2) is expressed in not only adipocytes and macrophages but also peritubular capillaries in the normal kidney. We recently demonstrated that ectopic expression of FABP4, but not FABP1 known as liver FABP (L-FABP), in the glomerulus is associated with progression of proteinuria and renal dysfunction. However, urinary excretion of FABP4 has not been investigated. Methods: Subjects who participated in the Tanno-Sobetsu Study, a study with a population-based cohort design, in 2011 (n=392, male/female: 166/226) were enrolled. Urinary FABP4 (U-FABP4) and urinary albumin-to-creatinine ratio (UACR) were measured. Change in estimated glomerular filtration rate (eGFR) was followed up one year later. Results: In 93 (23.7%) of the 392 subjects, U-FABP4 level was below the sensitivity of the assay. Subjects with undetectable U-FABP4 were younger and had lower UACR and higher eGFR levels than subjects with measurable U-FABP4. U-FABP4 level was positively correlated with age, systolic blood pressure and levels of serum FABP4 (S-FABP4), triglycerides, hemoglobin A1c (HbA1c), urinary FABP1 (U-FABP1) and UACR (r=0.360, p<0.001). Age, S-FABP4, U-FABP1 and UACR were independent predictors of U-FABP4. On the other hand, systolic blood pressure, HbA1c and U-FABP4 were independently correlated with UACR. Reduction in eGFR after one year was significantly larger in a group with the highest tertile of baseline U-FABP4 than a group with the lowest tertile. Conclusions: Urinary FABP4 level is independently correlated with level of albuminuria and possibly predicts yearly decline of eGFR. U-FABP4 would be a novel biomarker of glomerular damage.

DOI PubMed

Reduction of endoplasmic reticulum stress inhibits neointima formation after vascular injury

Shutaro Ishimura, Masato Furuhashi, Tomohiro Mita, Takahiro Fuseya, Yuki Watanabe, Kyoko Hoshina, Nobuaki Kokubu, Katsumi Inoue, Hideaki Yoshida, Tetsuji Miura

SCIENTIFIC REPORTS ( NATURE PUBLISHING GROUP ) 4 6943 2014.11 [Refereed]

Endoplasmic reticulum (ER) stress and inappropriate adaptation through the unfolded protein response (UPR) are predominant features of pathological processes. However, little is known about the link between ER stress and endovascular injury. We investigated the involvement of ER stress in neointima hyperplasia after vascular injury. The femoral arteries of 7-8-week-old male mice were subjected to wire-induced vascular injury. After 4 weeks, immunohistological analysis showed that ER stress markers were upregulated in the hyperplastic neointima. Neointima formation was increased by 54.8% in X-box binding protein-1 (XBP1) heterozygous mice, a model of compromised UPR. Knockdown of Xbp1 in human coronary artery smooth muscle cells (CASMC) in vitro promoted cell proliferation and migration. Furthermore, treatment with ER stress reducers, 4-phenylbutyrate (4-PBA) and tauroursodeoxycholic acid (TUDCA), decreased the intima-to-media ratio after wire injury by 50.0% and 72.8%, respectively. Chronic stimulation of CASMC with PDGF-BB activated the UPR, and treatment with 4-PBA and TUDCA significantly suppressed the PDGF-BB-induced ER stress markers in CASMC and the proliferation and migration of CASMC. In conclusion, increased ER stress contributes to neointima formation after vascular injury, while UPR signaling downstream of XBP1 plays a suppressive role. Suppression of ER stress would be a novel strategy against post-angioplasty vascular restenosis.

DOI PubMed

脂肪酸結合タンパク4はAC-PKAおよびGC-PKG経路を介して脂肪分解と共に脂肪細胞から分泌される

美田知宏, 古橋眞人, 石村周太郎, 伏屋敬博, 保科京香, 渡邊礼, 大野紘平, 田中希尚, 吉田英昭, 三浦哲嗣

肥満研究 ( (一社)日本肥満学会 ) 20 ( Suppl. ) 161 - 161 2014.10

アンジオテンシンII受容体拮抗薬による新規アディポカイン脂肪酸結合タンパク4濃度の変化

伏屋敬博, 古橋眞人, 美田知宏, 茂庭仁人, 渡邊礼, 大森晶奈, 大野紘平, 田中希尚, 石村周太郎, 吉田英昭, 三浦哲嗣

日本高血圧学会総会プログラム・抄録集 ( (NPO)日本高血圧学会 ) 37回 391 - 391 2014.10

Emerging issues in radiogenic cataracts and cardiovascular disease

Nobuyuki Hamada, Yuki Fujimichi, Toshiyasu Iwasaki, Noriko Fujii, Masato Furuhashi, Eri Kubo, Tohru Minamino, Takaharu Nomura, Hitoshi Sato

JOURNAL OF RADIATION RESEARCH ( OXFORD UNIV PRESS ) 55 ( 5 ) 831 - 846 2014.09 [Refereed]

In 2011, the International Commission on Radiological Protection issued a statement on tissue reactions (formerly termed non-stochastic or deterministic effects) to recommend lowering the threshold for cataracts and the occupational equivalent dose limit for the crystalline lens of the eye. Furthermore, this statement was the first to list circulatory disease (cardiovascular and cerebrovascular disease) as a health hazard of radiation exposure and to assign its threshold for the heart and brain. These changes have stimulated various discussions and may have impacts on some radiation workers, such as those in the medical sector. This paper considers emerging issues associated with cataracts and cardiovascular disease. For cataracts, topics dealt with herein include (i) the progressive nature, stochastic nature, target cells and trigger events of lens opacification, (ii) roles of lens protein denaturation, oxidative stress, calcium ions, tumor suppressors and DNA repair factors in cataractogenesis, (iii) dose rate effect, radiation weighting factor, and classification systems for cataracts, and (iv) estimation of the lens dose in clinical settings. Topics for cardiovascular disease include experimental animal models, relevant surrogate markers, latency period, target tissues, and roles of inflammation and cellular senescence. Future research needs are also discussed.

DOI PubMed

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Papers - FURUHASHI Masato