l-Arginine prevents inflammatory and pro-calcific differentiation of interstitial aortic valve cells

Rattazzi, Marcello; Donato, Maristella; Bertacco, Elisa; Millioni, Renato; Franchin, Cinzia; Mortarino, Cinzia; Faggin, Elisabetta; Nardin, Chiara; Scarpa, Riccardo; Cinetto, Francesco; Agostini, Carlo; Ferri, Nicola; Pauletto, Paolo; Arrigoni, Giorgio

doi:10.1016/j.atherosclerosis.2020.02.024

Cited by 19 publications

(19 citation statements)

References 30 publications

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“…In addition to the effects on the vasculature, NO donors seem to act directly in the valve; for example, L-Arginine and nitroprusside have been shown to inhibit osteogenic differentiation of cultured VICs [128,129]. This anti-calcific effect seems to be mediated by sGC activators (such as BAY and YC-1) or by agents increasing intracellular cGMP levels, while it is prevented by sGC inhibitors (such as ODQ), suggesting that the protective action of NO on VICs is probably dependent on the activation of the sGC/cGMP pathway [130,131]. Collectively, these findings motivate potential therapeutic strategies based on the activation of the NO/sGC/cGMP pathway, providing a rationale for clinical trials with NO donors and sGC activators to test this hypothesis.…”

Section: Current Evidencementioning

confidence: 99%

Current Evidence and Future Perspectives on Pharmacological Treatment of Calcific Aortic Valve Stenosis

Donato

Ferri

Lupo

et al. 2020

IJMS

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Calcific aortic valve stenosis (CAVS), the most common heart valve disease, is characterized by the slow progressive fibro-calcific remodeling of the valve leaflets, leading to progressive obstruction to the blood flow. CAVS is an increasing health care burden and the development of an effective medical treatment is a major medical need. To date, no effective pharmacological therapies have proven to halt or delay its progression to the severe symptomatic stage and aortic valve replacement represents the only available option to improve clinical outcomes and to increase survival. In the present report, the current knowledge and latest advances in the medical management of patients with CAVS are summarized, placing emphasis on lipid-lowering agents, vasoactive drugs, and anti-calcific treatments. In addition, novel potential therapeutic targets recently identified and currently under investigation are reported.

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Section: Current Evidencementioning

confidence: 99%

Current Evidence and Future Perspectives on Pharmacological Treatment of Calcific Aortic Valve Stenosis

Donato

Ferri

Lupo

et al. 2020

IJMS

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“…The results revealed a reduction in matrix calcification due to reduced ALP activity and calcium deposition. Besides, L-Arginine is able to reduce the inflammatory activation of cells [ 125 ]. It is known that the uncoupling of NOS is involved in the generation of superoxide; increased protein expression and functional activity of eNOS in rabbit aortic valves upon treatment with atorvastatin leads to diminished calcification and reduced oxidative stress and inflammation [ 126 ].…”

Section: Aortic Stenosis Pathobiology a Molecular Perspectivementioning

confidence: 99%

Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives

Pedriali

Morciano

Patergnani

et al. 2020

IJMS

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Calcific aortic stenosis is a disorder that impacts the physiology of heart valves. Fibrocalcific events progress in conjunction with thickening of the valve leaflets. Over the years, these events promote stenosis and obstruction of blood flow. Known and common risk factors are congenital defects, aging and metabolic syndromes linked to high plasma levels of lipoproteins. Inflammation and oxidative stress are the main molecular mediators of the evolution of aortic stenosis in patients and these mediators regulate both the degradation and remodeling processes. Mitochondrial dysfunction and dysregulation of autophagy also contribute to the disease. A better understanding of these cellular impairments might help to develop new ways to treat patients since, at the moment, there is no effective medical treatment to diminish neither the advancement of valve stenosis nor the left ventricular function impairments, and the current approaches are surgical treatment or transcatheter aortic valve replacement with prosthesis.

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“…The pathological results also indicated that the gastric mucosa of the CAG group exhibited submucosal edema, extensive atrophy, and reduced gastric glands, which were the key inflammatory features. Furthermore, our results indicated that SDG could alleviate CAG through inhibiting the levels of some inflammatory mediators ( l ‐arginine, arachidonic acid, and lipids) (Rattazzi et al, 2020; Sonnweber et al, 2018). In the CAG group, the levels of l ‐arginine and arachidonic acid increased obviously.…”

Section: Discussionmentioning

confidence: 77%

Explore the effects of Shidan granules on chronic atrophic gastritis using LC–MS based plasma metabolomics study

Wang

Jun-quan

et al. 2021

Biomedical Chromatography

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Shidan granule (SDG), a traditional Chinese medicine in‐hospital preparation, has been demonstrated to exert good effects on chronic atrophic gastritis (CAG) in clinics. However, the underlying mechanism of SDG against CAG is still unclear. This study utilized an untargeted plasma metabolomics approach to explore the potential mechanism of SDG in CAG rats using LC–MS and pattern recognition analysis. The results indicated that SDG could effectively improve the biochemical indexes and pathology features of CAG rats. Nineteen potential biomarkers (variable importance in projection > 1 and P < 0.05) contributing to CAG progress were identified. After SDG intervention, 17 biomarkers were obviously restored to normal levels. Further metabolic pathway analysis showed that aspartate and glutamate metabolism, arachidonic acid metabolism, arginine and proline metabolism, and TCA cycle were the most related pathways for SDG treatment. Based on these findings, the main mechanisms of SDG against CAG might be attributed to the regulatory effects of energy balance, inflammatory suppression, and improvement in disturbed amino acid and lipid metabolism. This study provided information for the mechanism research of SDG against CAG and would promote its clinical application.

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l-Arginine prevents inflammatory and pro-calcific differentiation of interstitial aortic valve cells

Cited by 19 publications

References 30 publications

Current Evidence and Future Perspectives on Pharmacological Treatment of Calcific Aortic Valve Stenosis

Current Evidence and Future Perspectives on Pharmacological Treatment of Calcific Aortic Valve Stenosis

Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives

Explore the effects of Shidan granules on chronic atrophic gastritis using LC–MS based plasma metabolomics study

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