Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria

Gabandé‐Rodríguez, Enrique; Heras, Manuel M. Gómez de las; Mittelbrunn, Marı́a

doi:10.3390/cells9010082

Cited by 67 publications

(31 citation statements)

References 201 publications

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“…Resveratrol can also increase SIRT3 and antioxidant enzymes, as shown in AD lymphocytes [160]. The effects of resveratrol, like the ketogenic diet, on mitochondrial function also has parallels to calorie restriction [161]. Resveratrol disinhibits PDC, thereby increasing acetyl-CoA and OXPHOS, as shown in the rodent cortex [162], indicating that it will activate the mitochondrial melatonergic pathway.…”

Section: Resveratrolmentioning

confidence: 95%

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease<strong> </strong>

Anderson¹,

Maes²

2020

Preprint

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Alzheimer's disease (AD) has been the subject of extensive investigation as to its biological underpinnings. However, this has produced little of therapeutic benefit or indeed provided any accepted biomarkers that could tailor treatment. This chapter reviews data on the main pathophysiologic processes that have been widely shown to be altered in AD, including circadian dysregulation, mitochondrial dysfunction, gut dysbiosis, and immune-glia-platelet activation. It is proposed that alterations in the gut microbiome, including gut dysbiosis and increased gut permeability drive changes in mitochondrial function that are intimately associated with significant variations in sirtuin expression. Both mitochondria-located and nucleus/cytoplasm located sirtuins can act on mitochondrial function in different cells and body systems to co-ordinate the ageing-associated changes that underpin AD. The sirtuins are therefore key aspect to a developmental model of AD that is more 'holistic' in perspective, thereby providing a framework for the detection of earlier biomarkers and more successful treatment for the heterogenous nature of AD pathoetiology.

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Section: Resveratrolmentioning

confidence: 95%

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease<strong> </strong>

Anderson¹,

Maes²

2020

Preprint

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“…This inflammatory reaction may contribute to facilitated muscle protein degradation. Calorie restriction and its mimetics, such as NAD + precursors, resveratrol, metformin, and rapamycin, appear to prevent inflammaging through modulating metabolic pathways including autophagy [130]. Induced autophagy via omega-3 PUFAs [129,131] may contribute to suppress inflammaging and delay the development of sarcopenia.…”

Section: Therapeutic Potential Of Dha In Sarcopenia By Modulating Upsmentioning

confidence: 99%

Docosahexaenoic Acid, a Potential Treatment for Sarcopenia, Modulates the Ubiquitin–Proteasome and the Autophagy–Lysosome Systems

2020

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One of the characteristic features of aging is the progressive loss of muscle mass, a nosological syndrome called sarcopenia. It is also a pathologic risk factor for many clinically adverse outcomes in older adults. Therefore, delaying the loss of muscle mass, through either boosting muscle protein synthesis or slowing down muscle protein degradation using nutritional supplements could be a compelling strategy to address the needs of the world’s aging population. Here, we review the recently identified properties of docosahexaenoic acid (DHA). It was shown to delay muscle wasting by stimulating intermediate oxidative stress and inhibiting proteasomal degradation of muscle proteins. Both the ubiquitin–proteasome and the autophagy–lysosome systems are modulated by DHA. Collectively, growing evidence indicates that DHA is a potent pharmacological agent that could improve muscle homeostasis. Better understanding of cellular proteolytic systems associated with sarcopenia will allow us to identify novel therapeutic interventions, such as omega-3 polyunsaturated fatty acids, to treat this disease.

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“…Currently, several compounds are under investigation for use in such therapies. These substances are generally referred to as CR mimetics 45,46 . Main characteristic features of these agents are as follows: (1) inducing metabolic, physiological, and hormonal effects similar to those induced by CR; (2) activating stress response pathways similarly to CR; (3) extending the lifespan and delaying the onset and/or reducing the incidence of aging‐associated disorders 44 .…”

Section: Caloric Restriction Mimeticsmentioning

confidence: 99%

Repurposing drugs to fight aging: The difficult path from bench to bedside

Vaiserman

Koliada

Lushchak

et al. 2020

Medicinal Research Reviews

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The steady rise in life expectancy occurred across all developed countries during the last century. This demographic trend is, however, not accompanied by the same healthspan extension. This is since aging is the main risk factor for all age‐associated pathological conditions. Therefore, slowing the rate of aging is suggested to be more efficient in preventing or delaying age‐related diseases than treat them one by one, which is the common approach in a current pharmacological disease‐oriented paradigm. To date, a variety of medications designed to treat particular pathological conditions have been shown to exhibit pro‐longevity effects in different experimental models. Among them, there are many commonly used prescription and over‐the‐counter pharmaceuticals such as metformin, rapamycin, aspirin, statins, melatonin, vitamin antioxidants, etc. All of them are being increasingly investigated in preclinical and clinical trials with the aim of determine whether they have potential for extension of human healthspan. The results from these trials are frequently inconclusive and fall short of initial expectations, suggesting that innovative research ideas and additional translational steps are required to overcome obstacles for implementation of such approaches in clinical practice. In this review, recent advances and challenges in the field of repurposing widely used conventional pharmaceuticals to target the aging process are summarized and discussed.

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Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria

Cited by 67 publications

References 201 publications

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease<strong> </strong>

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease<strong> </strong>

Docosahexaenoic Acid, a Potential Treatment for Sarcopenia, Modulates the Ubiquitin–Proteasome and the Autophagy–Lysosome Systems

Repurposing drugs to fight aging: The difficult path from bench to bedside

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Control of Inflammation by Calorie Restriction Mimetics: On the Crossroad of Autophagy and Mitochondria

Cited by 67 publications

References 201 publications

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer&rsquo;s Disease<strong> </strong>

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer&rsquo;s Disease<strong> </strong>

Docosahexaenoic Acid, a Potential Treatment for Sarcopenia, Modulates the Ubiquitin–Proteasome and the Autophagy–Lysosome Systems

Repurposing drugs to fight aging: The difficult path from bench to bedside

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Product

Resources

About

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease<strong> </strong>

Sirtuins, Mitochondria and the Melatonergic Pathway in Alzheimer’s Disease<strong> </strong>