Beneficial effects of a combination of natural product activators of autophagy on endothelial cells and platelets

Carnevale, Roberto; Nocella, Cristina; Schiavon, Sonia; Cammisotto, Vittoria; Cotugno, Maria; Forte, Maurizio; Valenti, Valentina; Marchitti, Simona; Vecchio, Danièle; Zoccai, Giuseppe Biondi; Rubattu, Speranza; Martinelli, Ombretta; Pignatelli, Pasquale; Violi, Francesco; Volpe, Massimo; Versaci, Francesco; Frati, Luigi; Frati, Giacomo; Sciarretta, Sebastiano

doi:10.1111/bph.15399

Cited by 19 publications

(21 citation statements)

References 35 publications

(58 reference statements)

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“…Interestingly, we found that increased Nox2 activity and oxidative stress were associated with autophagy inhibition, confirming previous evidence demonstrating that oxidative stress inhibits autophagy ( 22 ). Autophagy is an intracellular degradation mechanism playing a paramount adaptive cellular modification in response to oxidative stress, characterized by elimination of excessive cellular ROS and maintenance of an appropriate redox balance.…”

Section: Discussionsupporting

confidence: 91%

“…Lastly, natural activators of autophagy are under investigation in the setting of several cardiovascular diseases with results of paramount importance ( 22 , 26 , 27 ). Interestingly, a recent work demonstrated that oral spermidine supplementation increases plasma spermidine levels and suppresses the development of experimental abdominal aortic aneurysms with preservation of aortic structural integrity by reducing inflammatory cell infiltration and circulating inflammatory monocytes, as well as increasing autophagy-related protein ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

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Role of Oxidative Stress and Autophagy in Thoracic Aortic Aneurysms

Irace¹,

Cammisotto²,

Valenti³

et al. 2021

JACC: Basic to Translational Science

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Role of Oxidative Stress and Autophagy in Thoracic Aortic Aneurysms

Irace¹,

Cammisotto²,

Valenti³

et al. 2021

JACC: Basic to Translational Science

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“…Thus, stimulating glucose oxidation will amplify the effect of CR-mimetics by enhancing ATP production in concert with improving systemic glucose tolerance and inflammation. This notion can be further supported by others showing that a combination of spermidine from a natural product with nicotinamide inhibits oxidative stress and improves endothelial cell survival, in a potentiated manner than each compound alone, in platelets isolated from patients with metabolic syndrome [ 259 ]. This also holds true for the effect of combinational resveratrol-piperine with α-tocopherol (has an anti-inflammatory activity [ 260 ]), in a clinical trial [ 47 ], in which, the decrease in arterial hypertension and inflammation is evident in older patients [age (68 ± 4.7) years] with metabolic syndrome [ 47 ].…”

Section: Perspectivementioning

confidence: 80%

Caloric restriction-mimetics for the reduction of heart failure risk in aging heart: with consideration of gender-related differences

et al. 2022

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The literature is full of claims regarding the consumption of polyphenol or polyamine-rich foods that offer some protection from developing cardiovascular disease (CVD). This is achieved by preventing cardiac hypertrophy and protecting blood vessels through improving the function of endothelium. However, do these interventions work in the aged human hearts? Cardiac aging is accompanied by an increase in left ventricular hypertrophy, along with diastolic and systolic dysfunction. It also confers significant cardiovascular risks for both sexes. The incidence and prevalence of CVD increase sharply at an earlier age in men than women. Furthermore, the patterns of heart failure differ between sexes, as do the lifetime risk factors. Do caloric restriction (CR)-mimetics, rich in polyphenol or polyamine, delay or reverse cardiac aging equally in both men and women? This review will discuss three areas: (1) mechanisms underlying age-related cardiac remodeling; (2) gender-related differences and potential mechanisms underlying diminished cardiac response in older men and women; (3) we select a few polyphenol or polyamine rich compounds as the CR-mimetics, such as resveratrol, quercetin, curcumin, epigallocatechin gallate and spermidine, due to their capability to extend health-span and induce autophagy. We outline their abilities and issues on retarding aging in animal hearts and preventing CVD in humans. We discuss the confounding factors that should be considered for developing therapeutic strategies against cardiac aging in humans.

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“… 10 , 77 Therefore, autophagy occur in ECs in response to hypoxia or serum depletion is necessary for angiogenic behaviour, 89 and activation of autophagy could improve ECs survival and function by alleviating oxidative stress. 90 Lack of endothelial the glucocorticoid receptor (GR) triggers autophagy flux, which will lead to activation of Wnt/β‐catenin signalling and promote angiogenesis. 91 In a muscle injury mouse model induced by hindlimb ischaemia, the autophagy pathway was induced under prolonged hypoxia in ECs, which could increase the angiogenic activities of ECs under tissue regeneration and consequently helps regeneration of surrounding tissues.…”

Section: Autophagy In Non‐myogenic Cellsmentioning

confidence: 99%

Autophagy in muscle regeneration: potential therapies for myopathies

Chen

Liu

et al. 2022

J cachexia sarcopenia muscle

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Autophagy classically functions as a physiological process to degrade cytoplasmic components, protein aggregates, and/or organelles, as a mechanism for nutrient breakdown, and as a regulator of cellular architecture. Its biological functions include metabolic stress adaptation, stem cell differentiation, immunomodulation and diseases regulation, and so on. Current researches have proved that autophagy dysfunction may contribute to the pathogenesis of some myopathies through impairment of myofibres regeneration. Studies of autophagy inhibition also indicate the importance of autophagy in muscle regeneration, while activation of autophagy can restore muscle function in some myopathies. In this review, we aim to report the mechanisms of action of autophagy on muscle regeneration to provide relevant references for the treatment of regenerating defective myopathies by regulating autophagy. Results have shown that one key mechanism of autophagy regulating the muscle regeneration is to affect the differentiation fate of muscle stem cells (MuSCs), including quiescence maintenance, activation and differentiation. The roles of autophagy (organelle/protein degradation, energy facilitation, and/or other) vary at different myogenic stages of the repair process. When the muscle is in homeostasis, basal autophagy can maintain the quiescence state and stemness of MuSCs by renewing organelle and protein. After injury, the increased autophagy flux contributes to meet biological energy demand of MuSCs during activation and proliferation. By mitochondrial remodelling, autophagy during differentiation can promote the metabolic transformation and balance mitochondrial‐mediated apoptosis signals in myoblasts. Autophagy in mature myofibres is also essential for the degradation of necrotic myofibres, and may affect the dynamics of MuSCs by affecting the secretion spectrum of myofibres or the recruitment of supporting cells. Except for myogenic cells, autophagy also plays an important role in regulating the function of non‐myogenic cells in the muscle microenvironment, which is also essential for successful muscle recovery. Autophagy can regulate the immune microenvironment during muscle regeneration through the recruitment and polarization of macrophages, while autophagy in endothelial cells can regulate muscle regeneration in an angiogenic or angiogenesis‐independent manner. Drug or nutrition targeted autophagy has been preliminarily proved to restore muscle function in myopathies by promoting muscle regeneration, and further understanding the role and mechanism of autophagy in various cell types during muscle regeneration will enable more effective combinatorial therapeutic strategies.

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Beneficial effects of a combination of natural product activators of autophagy on endothelial cells and platelets

Cited by 19 publications

References 35 publications

Role of Oxidative Stress and Autophagy in Thoracic Aortic Aneurysms

Role of Oxidative Stress and Autophagy in Thoracic Aortic Aneurysms

Caloric restriction-mimetics for the reduction of heart failure risk in aging heart: with consideration of gender-related differences

Autophagy in muscle regeneration: potential therapies for myopathies

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