Angiotensin II receptor blocker inhibits abnormal accumulation of advanced glycation end products and retinal damage in a rat model of type 2 diabetes

Sugiyama, Tetsuya; Okuno, Takashi; Fukuhara, Masayuki; Oku, Hidehiro; Ikeda, Tsunehiko; Obayashi, Hiroshi; Ohta, Mitsuhiro; Fukui, Michiaki; Hasegawa, Goji; Nakamura, Naoto

doi:10.1016/j.exer.2007.06.008

Cited by 54 publications

(43 citation statements)

References 23 publications

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“…The blood glucose levels were determined using Glutest Neo (Sanwa Kagaku Kenkyusho Co., Ltd., Nagoya), as previously described (16). MABP was measured using an automatic sphygmomanometer (BP Monitor for Rats and Mice Model MK-2000; Muromachi Kikai Co., Ltd., Tokyo).…”

Section: Measurement Of Body Weight (Bw) Mean Arterial Blood Pressurmentioning

confidence: 99%

Long-Term Angiotensin II Blockade May Improve Not Only Hyperglycemia but Also Age-Associated Cardiac Fibrosis

et al. 2009

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Abstract. In the present study, the effects of long-term angiotensin (Ang) II antagonism on the development of cardiac and endothelial disorders were examined in Spontaneously Diabetic Torii (SDT) rats. Blood glucose concentration started to increase markedly in the untreated SDT rats from 20 weeks of age, while the blood glucose concentrations of candesartan cilexetil-treated SDT rats were significantly lower until 30 weeks of age. Cardiac function deteriorated in SDT rats and was accompanied by severe cardiac fibrosis, cardiac hypertrophy, and microstructural pathologic change in cardiomyocytes. Cardiac function was very well preserved in the agematched Sprague Dawley (SD) rats, but cardiac fibrosis developed with aging. Candesartan cilexetil treatment improved cardiac structural remodeling and cardiac function in SDT rats. Surprisingly, the degree of cardiac fibrosis in candesartan cilexetil-treated SDT rats was less than that of SD rats. Immunohistological staining confirmed that in addition to collagen deposition, fibroblasts and myofibroblasts were the main cellular components in the cardiac fibrotic areas. The diabetic hearts showed positive staining for ACE, Ang II, and AT 1 receptors. SDT rats also showed decreased endothelial function, which was improved with candesartan cilexetil treatment. These findings indicate that Ang II is involved in the development of cardiac dysfunction by accelerating cardiac remodeling and cardiomyocyte damage in the presence of hyperglycemia. On the other hand, although the mechanisms responsible for the cardiac fibrosis that occurs under normal conditions may differ greatly from those responsible for cardiac fibrosis with hyperglycemia, Ang II seems to play an important role in both.

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Section: Measurement Of Body Weight (Bw) Mean Arterial Blood Pressurmentioning

confidence: 99%

Long-Term Angiotensin II Blockade May Improve Not Only Hyperglycemia but Also Age-Associated Cardiac Fibrosis

et al. 2009

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“…Further, candesartan treatment decreased diabetes-stimulated retinal vascular permeability suggesting that activation of AT1R contributes to BRB dysfunction (Phipps et al, 2009) and at the same time significantly reduced the levels of VEGF and NADPH oxidase subunits in type 2 DR (Fukumoto et al, 2008). Candesartan also inhibited the development of DR by reducing the accumulation of pentosidine (an AGE) and expression of VEGF (Sugiyama et al, 2007). To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi.…”

Section: P1030mentioning

confidence: 99%

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

Szabadfi

Pintér

Reglődi

et al. 2014

International Review of Cell and Molecular Biology

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Any queries or remarks that have arisen during the processing of your manuscript are listed below and are highlighted by flags in the proof. (AU indicates author queries; ED indicates editor queries; and TS/TY indicates typesetter queries.) Please check your proof carefully and answer all AU queries. Mark all corrections and query answers at the appropriate place in the proof (e.g., by using on-screen annotation in the PDF file http:// www.elsevier.com/book-authors/science-and-technology-book-publishing/overviewof-the-publishing-process) or compile them in a separate list, and tick off below to indicate that you have answered the query. Please return your input as instructed by the project manager. Location in ChapterQuery / remark AU:1, page 47 Please check the change made in the table title. AU:2, page 57 Citation " Frank et al. (1997)" has not been found in the reference list. Please supply full details for this reference. AU:3, page 58Citation "Wang et al. (2004)" has not been found in the reference list. Please supply full details for this reference. AU:4, page 63The citation "Wang et al. (2010)" has been changed to " Wang et al. (2010)" to match the author name/date in the reference list. Please check here and in subsequent occurrences, and correct if necessary. AU:5, page 3The abbreviations IBA-1 and ZFDM are used only once in the text and they have been deleted in the text. Please consider deleting them from the abbreviation list. B978-0-12-800179-0.00001-5, 00001 IRCMB, 978-0-12-800179-0To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. AU:6, page 3Please check if all occurrences of "interstitial cell adhesion molecule 1" should be changed to "intercellular adhesion molecule 1." AU:7, page 3Please check the change from "neural" to "neuronal" to match with the text.AU:8, page 3The abbreviation "PKCa" is not used in the text. Please check and delete from the abbreviation list. AU:9, page 9Please check if "retinal ganglion cells (RGCs)" is okay as edited.AU:10, page 13 Please check the change from "retinal circuity" to "retinal circuitry."AU:11, page 17 Please check if "polyamine catabolism" is okay as edited. AU:20, page 46 Please check if edit to sentence starting "The STZ-induced diabetic. . ." is okay. B978-0-12-800179-0.00001-5, 00001 IRCMB, 978-0-12-800179-0To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter SPi. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. AU:21, page 72Please check if "SST" is okay as edited.AU:2...

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“…Kim et al [45] showed that perindopril (an ACE inhibitor) attenuated VEGFmediated BRB breakdown in rats with streptozotocininduced diabetes mellitus (STZ-DM). It is also noteworthy that candesartan (an AT-R blocker) inhibited retinal accumulation of the AGE product pentosidine in spontaneously diabetic Torii rats [46]. Besides reducing microvascular disease, recent research points to neuroprotection as a relevant mechanism involved in the beneficial effects of AT-R blockers in DR [47][48][49].…”

Section: Mechanisms Of Actionmentioning

confidence: 99%

“…(3) [41][42][43][44][45][46][47][48][49]. Angiotensin II (AT) binds and activates two primary receptors, AT1-R and AT2-R.…”

Section: Mechanisms Of Actionmentioning

confidence: 99%

Non-Traditional Systemic Treatments for Diabetic Retinopathy: An Evidence-Based Review

Simó

Ballarini²,

Cunha‐Vaz³

et al. 2015

CMC

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Abstract:The rapid escalation in the global prevalence diabetes, with more than 30% being afflicted with diabetic retinopathy (DR), means it is likely that associated vision-threatening conditions will also rise substantially. This means that new therapeutic approaches need to be found that go beyond the current standards of diabetic care, and which are effective in the early stages of the disease. In recent decades several new pharmacological agents have been investigated for their effectiveness in preventing the appearance and progression of DR or in reversing DR; some with limited success while others appear promising. This up-to-date critical review of non-traditional systemic treatments for DR is based on the published evidence in MEDLINE spanning 1980-December 2014. It discusses a number of therapeutic options, paying particular attention to the mechanisms of action and the clinical evidence for the use of renin-angiotensin system blockade, fenofibrate and calcium dobesilate monohydrate in DR.

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Angiotensin II receptor blocker inhibits abnormal accumulation of advanced glycation end products and retinal damage in a rat model of type 2 diabetes

Cited by 54 publications

References 23 publications

Long-Term Angiotensin II Blockade May Improve Not Only Hyperglycemia but Also Age-Associated Cardiac Fibrosis

Long-Term Angiotensin II Blockade May Improve Not Only Hyperglycemia but Also Age-Associated Cardiac Fibrosis

Neuropeptides, Trophic Factors, and Other Substances Providing Morphofunctional and Metabolic Protection in Experimental Models of Diabetic Retinopathy

Non-Traditional Systemic Treatments for Diabetic Retinopathy: An Evidence-Based Review

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