Institution
Kanazawa Medical University
Education•Kanazawa, Japan•
About: Kanazawa Medical University is a education organization based out in Kanazawa, Japan. It is known for research contribution in the topics: Population & Cancer. The organization has 3103 authors who have published 6322 publications receiving 144592 citations. The organization is also known as: Kanazawa ika daigaku.
Topics: Population, Cancer, Diabetes mellitus, Lung cancer, Blood pressure
Papers published on a yearly basis
Papers
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TL;DR: The activation of SIRT1 in the kidney may be a new therapeutic target to increase resistance to many causal factors in the development of renal diseases, including diabetic nephropathy.
Abstract: Sirtuins are members of the Sir2 (silent information regulator 2) family, a group of class III deacetylases. Mammals have seven different sirtuins, SIRT1–SIRT7. Among them, SIRT1, SIRT3 and SIRT6 are induced by calorie restriction conditions and are considered anti-aging molecules. SIRT1 has been the most extensively studied. SIRT1 deacetylates target proteins using the coenzyme NAD+ and is therefore linked to cellular energy metabolism and the redox state through multiple signalling and survival pathways. SIRT1 deficiency under various stress conditions, such as metabolic or oxidative stress or hypoxia, is implicated in the pathophysiologies of age-related diseases including diabetes, cardiovascular diseases, neurodegenerative disorders and renal diseases. In the kidneys, SIRT1 may inhibit renal cell apoptosis, inflammation and fibrosis, and may regulate lipid metabolism, autophagy, blood pressure and sodium balance. Therefore the activation of SIRT1 in the kidney may be a new therapeutic target to increase resistance to many causal factors in the development of renal diseases, including diabetic nephropathy. In addition, SIRT3 and SIRT6 are implicated in age-related disorders or longevity. In the present review, we discuss the protective functions of sirtuins and the association of sirtuins with the pathophysiology of renal diseases, including diabetic nephropathy.
191 citations
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TL;DR: Restoring the renoprotective action of autophagy in proximal tubules may improve renal outcomes in obese patients and enhance the understanding of obesity-related cell vulnerability in the kidneys.
Abstract: Obesity is an independent risk factor for renal dysfunction in patients with CKDs, including diabetic nephropathy, but the mechanism underlying this connection remains unclear. Autophagy is an intracellular degradation system that maintains intracellular homeostasis by removing damaged proteins and organelles, and autophagy insufficiency is associated with the pathogenesis of obesity-related diseases. We therefore examined the role of autophagy in obesity-mediated exacerbation of proteinuria-induced proximal tubular epithelial cell damage in mice and in human renal biopsy specimens. In nonobese mice, overt proteinuria, induced by intraperitoneal free fatty acid–albumin overload, led to mild tubular damage and apoptosis, and activated autophagy in proximal tubules reabsorbing urinary albumin. In contrast, diet-induced obesity suppressed proteinuria-induced autophagy and exacerbated proteinuria-induced tubular cell damage. Proximal tubule-specific autophagy-deficient mice, resulting from an Atg5 gene deletion, subjected to intraperitoneal free fatty acid–albumin overload developed severe proteinuria-induced tubular damage, suggesting that proteinuria-induced autophagy is renoprotective. Mammalian target of rapamycin (mTOR), a potent suppressor of autophagy, was activated in proximal tubules of obese mice, and treatment with an mTOR inhibitor ameliorated obesity-mediated autophagy insufficiency. Furthermore, both mTOR hyperactivation and autophagy suppression were observed in tubular cells of specimens obtained from obese patients with proteinuria. Thus, in addition to enhancing the understanding of obesity-related cell vulnerability in the kidneys, these results suggest that restoring the renoprotective action of autophagy in proximal tubules may improve renal outcomes in obese patients.
191 citations
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TL;DR: It was found that HCV-PT, the prototype reported from the U.S.A., was rare in Japan, suggesting that distribution of HCV genotypes may be different in various countries, and the prevalence of HCVs genotypes was compared in different countries.
188 citations
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University of Cambridge1, St George's, University of London2, Harvard University3, The Heart Research Institute4, Group Health Cooperative5, German Cancer Research Center6, University of Paris-Sud7, French Institute of Health and Medical Research8, University of Bristol9, Yamagata University10, Innsbruck Medical University11, University College London12, University of Pittsburgh13, University of Edinburgh14, Uppsala University15, University of Western Australia16, Queen Mary University of London17, University of Groningen18, University of Glasgow19, Sheba Medical Center20, Cardiff University21, University of New South Wales22, University of Gothenburg23, Medical University of South Carolina24, Duke University25, Yeshiva University26, Istanbul University27, University of Padua28, Leiden University29, University of Texas Health Science Center at Houston30, Istituto Superiore di Sanità31, University of Copenhagen32, Norwegian Institute of Public Health33, Umeå University34, University of Eastern Finland35, University of Helsinki36, North Shore-LIJ Health System37, University of California, San Diego38, Erasmus University Rotterdam39, University of Iceland40, Rush University Medical Center41, University of Iowa42, University of Vermont43, Boston University44, Georgetown University45, Kyushu University46, Kanazawa Medical University47, Howard University48, Utrecht University49, Johns Hopkins University50
TL;DR: The improvement provided by HbA1c assessment in prediction of CVD risk was equal to or better than estimated improvements for measurement of fasting, random, or postload plasma glucose levels.
Abstract: IMPORTANCE The value of measuring levels of glycated hemoglobin (HbA(1c)) for the prediction of first cardiovascular events is uncertain. OBJECTIVE To determine whether adding information on HbA(1c ...
185 citations
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15 Oct 2016TL;DR: The activation of Sirt1 in vascular tissue, which includes ECs, monocytes/macrophages and VSMCs, may be a new therapeutic strategy against atherosclerosis and the increasing resistance to the metabolic disorder-related causal factors of CVD.
Abstract: Cardiovascular disease (CVD) due to atherosclerosis is the main cause of death in both the elderly and patients with metabolic diseases, including diabetes. Aging processes contribute to the pathogenesis of atherosclerosis. Calorie restriction (CR) is recognized as a dietary intervention for promoting longevity and delaying age-related diseases, including atherosclerosis. Sirt1, an NAD+-dependent deacetylase, is considered an anti-aging molecule and is induced during CR. Sirt1 deacetylates target proteins and is linked to cellular metabolism, the redox state and survival pathways. Sirt1 expression/activation is decreased in vascular tissue undergoing senescence. Sirt1 deficiency in endothelial cells (ECs), vascular smooth muscle cells (VSMCs) and monocytes/macrophages contributes to increased oxidative stress, inflammation, foam cell formation, senescences impaired nitric oxide production and autophagy, thereby promoting vascular aging and atherosclerosis. Endothelial dysfunction, activation of monocytes/macrophages, and the functional and phenotypical plasticity of VSMCs are critically implicated in the pathogenesis of atherosclerosis through multiple mechanisms. Therefore, the activation of Sirt1 in vascular tissue, which includes ECs, monocytes/macrophages and VSMCs, may be a new therapeutic strategy against atherosclerosis and the increasing resistance to the metabolic disorder-related causal factors of CVD. In this review, we discuss the protective role of Sirt1 in the pathophysiology of vascular aging and atherosclerosis.
184 citations
Authors
Showing all 3113 results
Name | H-index | Papers | Citations |
---|---|---|---|
Michael Marmot | 193 | 1147 | 170338 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Zena Werb | 168 | 473 | 122629 |
Toshio Hirano | 120 | 401 | 55721 |
John T. Isaacs | 88 | 356 | 28217 |
Hiroshi Sasaki | 76 | 644 | 24222 |
Takuji Tanaka | 75 | 490 | 20946 |
Hiroshi Shimizu | 71 | 1368 | 26668 |
Daisuke Koya | 67 | 294 | 18746 |
Masashi Tanaka | 65 | 396 | 17110 |
Masashi Akiyama | 65 | 685 | 16404 |
Masayoshi Takeuchi | 64 | 279 | 13651 |
Takashi Yoshida | 63 | 328 | 13680 |
Tsutomu Hatano | 61 | 299 | 13668 |