Vitamin E protection of obesity-enhanced vascular calcification in uremic rats

Peralta-Ramírez, Alan; de, Addy Montes; Raya, Ana I.; Pineda, Carmen; López, Ignacio; Guerrero, Fatima; Diez, E.; Muñoz‐Castañeda, Juan R.; Martinez, Jean; Almadén, Yolanda; Rodríguez, Mariano; Aguilera–Tejero, Escolástico

doi:10.1152/ajprenal.00355.2013

Cited by 24 publications

(27 citation statements)

References 37 publications

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“…(11,46) We observed increased oxidative stress in our CKD animals compared to normal littermates, but no effect of ALT-711 to reduce oxidative stress. In the adenine-induced CKD and 5/6 th nephrectomy and obese rat models, arterial calcification was prevented by the antioxidants tempol (47) and vitamin E, (48) similar to our findings of decreased calcification at 3 mg/ kg of ALT-711. In contrast, we failed to see any effect on vascular calcification with N-acetylcysteine in the Cy/+ model (Authors and colleagues, unpublished data) or high-dose ALT-711.…”

Section: Discussionsupporting

confidence: 90%

Effect of Advanced Glycation End-Products (AGE) Lowering Drug ALT-711 on Biochemical, Vascular, and Bone Parameters in a Rat Model of CKD-MBD

Chen

Srinivasan

O’Neill

et al. 2019

Journal of Bone and Mineral Research

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Chronic kidney disease–mineral bone disorder (CKD‐MBD) is a systemic disorder that affects blood measures of bone and mineral homeostasis, vascular calcification, and bone. We hypothesized that the accumulation of advanced glycation end‐products (AGEs) in CKD may be responsible for the vascular and bone pathologies via alteration of collagen. We treated a naturally occurring model of CKD‐MBD, the Cy/+ rat, with a normal and high dose of the AGE crosslink breaker alagebrium (ALT‐711), or with calcium in the drinking water to mimic calcium phosphate binders for 10 weeks. These animals were compared to normal (NL) untreated animals. The results showed that CKD animals, compared to normal animals, had elevated blood urea nitrogen (BUN), PTH, FGF23 and phosphorus. Treatment with ALT‐711 had no effect on kidney function or PTH, but 3 mg/kg lowered FGF23 whereas calcium lowered PTH. Vascular calcification of the aorta assessed biochemically was increased in CKD animals compared to NL, and decreased by the normal, but not high dose of ALT‐711, with parallel decreases in left ventricular hypertrophy. ALT‐711 (3 mg/kg) did not alter aorta AGE content, but reduced aorta expression of receptor for advanced glycation end products (RAGE) and NADPH oxidase 2 (NOX2), suggesting effects related to decreased oxidative stress at the cellular level. The elevated total bone AGE was decreased by 3 mg/kg ALT‐711 and both bone AGE and cortical porosity were decreased by calcium treatment, but only calcium improved bone properties. In summary, treatment of CKD‐MBD with an AGE breaker ALT‐711, decreased FGF23, reduced aorta calcification, and reduced total bone AGE without improvement of bone mechanics. These results suggest little effect of ALT‐711 on collagen, but potential cellular effects. The data also highlights the need to better measure specific types of AGE proteins at the tissue level in order to fully elucidate the impact of AGEs on CKD‐MBD. © 2019 American Society for Bone and Mineral Research.

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Section: Discussionsupporting

confidence: 90%

Effect of Advanced Glycation End-Products (AGE) Lowering Drug ALT-711 on Biochemical, Vascular, and Bone Parameters in a Rat Model of CKD-MBD

Chen

Srinivasan

O’Neill

et al. 2019

Journal of Bone and Mineral Research

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“…An interesting characteristic of the cases reported here is that this product was not markedly increased, due mostly to the small elevation in serum phosphorus concentration. Another remarkable feature is that, when compared with experimental models of uremia-associated extraskeletal calcifications [ 28 ], vascular calcification was moderate. Widespread soft tissue mineralization, similar to what we are reporting here, has been recently described in three tigers which died in zoological gardens.…”

Section: Discussionmentioning

confidence: 99%

Chronic Vitamin D Intoxication in Captive Iberian Lynx (Lynx pardinus)

et al. 2016

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To document the biochemical and pathologic features of vitamin D intoxication in lynx and to characterize mineral metabolism in healthy lynx, blood samples were obtained from 40 captive lynx that had been receiving excessive (approximately 30 times the recommended dose) vitamin D3 in the diet, and from 29 healthy free ranging lynx. Tissue samples (kidney, stomach, lung, heart and aorta) were collected from 13 captive lynx that died as a result of renal disease and from 3 controls. Vitamin D intoxication resulted in renal failure in most lynx (n = 28), and widespread extraskeletal calcification was most severe in the kidneys and less prominent in cardiovascular tissues. Blood minerals and calciotropic hormones in healthy lynx were similar to values reported in domestic cats except for calcitriol which was higher in healthy lynx. Changes in mineral metabolism after vitamin D intoxication included hypercalcemia (12.0 ± 0.3 mg/dL), hyperphosphatemia (6.3 ± 0.4 mg/dL), increased plasma calcidiol (381.5 ± 28.2 ng/mL) and decreased plasma parathyroid hormone (1.2 ± 0.7 pg/mL). Hypercalcemia and, particularly, hyperphosphatemia were of lower magnitude that what has been previously reported in the course of vitamin D intoxication in other species. However, extraskeletal calcifications were severe. The data suggest that lynx are sensitive to excessive vitamin D and extreme care should be taken when supplementing this vitamin in captive lynx diets.

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“…Dietary L-lysine, vitamin E, and iron effectively reduce vascular calcification in animal models [53,54]. …”

Section: Strategies To Reduce Vascular Calcification and Their Effectmentioning

confidence: 99%

The Role of Vascular Calcification in Heart Failure and Cognitive Decline

Cheng

Wang

2017

Pulse

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Vascular calcification is heterogeneous and triggered by multiple mechanisms. It has been implicated in the development of heart failure with preserved ejection fraction (HFpEF) and cognitive function impairment. Understanding the pathophysiology of vascular calcification may help us improve the management of HFpEF, atherosclerosis, accelerated arterial stiffness, hypertension, and cognitive dysfunction. Currently, there are no effective strategies for treating accelerated arterial stiffness. This may indicate that once arterial stiffness or vascular calcification has developed, it may be less likely to stop the ongoing pathophysiology. Therefore, earlier intervention targeting the probable pathways of vascular calcification may benefit the patients with vascular calcification and related pathological conditions. In this review, we briefly discuss the proposed pathophysiological roles of vascular calcification in the development of heart failure and cognitive decline, the animal models used to study the link between vascular calcification and cardiovascular diseases, and the possible corresponding management strategies.

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Vitamin E protection of obesity-enhanced vascular calcification in uremic rats

Cited by 24 publications

References 37 publications

Effect of Advanced Glycation End-Products (AGE) Lowering Drug ALT-711 on Biochemical, Vascular, and Bone Parameters in a Rat Model of CKD-MBD

Effect of Advanced Glycation End-Products (AGE) Lowering Drug ALT-711 on Biochemical, Vascular, and Bone Parameters in a Rat Model of CKD-MBD

Chronic Vitamin D Intoxication in Captive Iberian Lynx (Lynx pardinus)

The Role of Vascular Calcification in Heart Failure and Cognitive Decline

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