SS‐31 and NMN: Two paths to improve metabolism and function in aged hearts

Whitson, Jeremy; Bitto, Alessandro; Zhang, Huiliang; Sweetwyne, Mariya T.; Coig, Rene; Bhayana, Saakshi; Shankland, Eric G.; Wang, Lu; Bammler, Theo K.; Mills, Kathryn F.; Imai, Shoichi; Conley, Kevin E.; Marcinek, David J.; Rabinovitch, Peter S.

doi:10.1111/acel.13213

Cited by 45 publications

(50 citation statements)

References 45 publications

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“…The National Institutes of Health and other organizations have made it a priority to fund research into microvascular contributions to the pathogenesis of VCI and AD, including the role of hypertension-induced microvascular damage. New therapeutic strategies aimed at reversing ageing-induced and hypertension-induced cardiovascular and cerebromicrovascular impairment include use of mitochondrial antioxidants 153 , 179 , polyphenols and other activators of NRF2 and sirtuin 1 (refs 150 , 180 ), senolytics 181 – 184 , anti-inflammatory interventions 185 , agents that rescue cellular energetics 128 , 186 and/or prevent cellular NAD + depletion 135 , 152 , AMPK activators 187 and mTOR inhibitors 188 .…”

Section: Future Perspectivesmentioning

confidence: 99%

Hypertension-induced cognitive impairment: from pathophysiology to public health

et al. 2021

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Hypertension affects two-thirds of people aged >60 years and significantly increases the risk of both vascular cognitive impairment and Alzheimer’s disease. Hypertension compromises the structural and functional integrity of the cerebral microcirculation, promoting microvascular rarefaction, cerebromicrovascular endothelial dysfunction and neurovascular uncoupling, which impair cerebral blood supply. In addition, hypertension disrupts the blood–brain barrier, promoting neuroinflammation and exacerbation of amyloid pathologies. Ageing is characterized by multifaceted homeostatic dysfunction and impaired cellular stress resilience, which exacerbate the deleterious cerebromicrovascular effects of hypertension. Neuroradiological markers of hypertension-induced cerebral small vessel disease include white matter hyperintensities, lacunar infarcts and microhaemorrhages, all of which are associated with cognitive decline. Use of pharmaceutical and lifestyle interventions that reduce blood pressure, in combination with treatments that promote microvascular health, have the potential to prevent or delay the pathogenesis of vascular cognitive impairment and Alzheimer’s disease in patients with hypertension.

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Section: Future Perspectivesmentioning

confidence: 99%

Hypertension-induced cognitive impairment: from pathophysiology to public health

et al. 2021

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“…NMN likely has a different mechanism of action than SS-31, as it works on NAD + biosynthesis to enhance mitochondrial function. 117 Because NMN and SS-31 work via distinct mechanisms, Whitson et al combined SS-31 and NMN treatments and reported that the two drugs in combination were more effective in treating heart dysfunction than either alone. 117 This provides new insight into treatment of tendinopathy by protecting mitochondria via NAPDH synthesis.…”

Section: Mitochondrial Protectants As Therapeutic Agentsmentioning

confidence: 99%

“…NMN appeared to have a greater acute effect on the heart than SS‐31 in this study. NMN likely has a different mechanism of action than SS‐31, as it works on NAD + biosynthesis to enhance mitochondrial function 117 . Because NMN and SS‐31 work via distinct mechanisms, Whitson et al .…”

Section: Mitochondrial Protectants As Therapeutic Agentsmentioning

confidence: 99%

Mitochondrial dysfunction and potential mitochondrial protectant treatments in tendinopathy

Zhang

Eliasberg

Rodeo

2021

Annals of the New York Academy of Sciences

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Tendinopathy is a common musculoskeletal condition that affects a wide range of patients, including athletes, laborers, and older patients. Tendinopathy is often characterized by pain, swelling, and impaired performance and function. The etiology of tendinopathy is multifactorial, including both intrinsic and extrinsic mechanisms. Various treatment strategies have been described, but outcomes are often variable, as tendons have poor intrinsic healing potential compared with other tissues. Therefore, several novel targets for tendon regeneration have been identified and are being explored. Mitochondria are organelles that generate adenosine triphosphate, and they are considered to be the power generators of the cell. Recently, mitochondrial dysfunction verified by increased reactive oxygen species (ROS), decreased superoxide dismutase activity, cristae disorganization, and decreased number of mitochondria has been identified as a mechanism that may contribute to tendinopathy. This has provided new insights for studying tendinopathy pathogenesis and potential treatments via antioxidant, metabolic modulation, or ROS inhibition. In this review, we present the current understanding of mitochondrial dysfunction in tendinopathy. The review summarizes the potential mechanism by which mitochondrial dysfunction contributes to the development of tendinopathy, as well as the potential therapeutic benefits of mitochondrial protectants in the treatment of tendinopathy.

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“…Nutritional stress, in the form of high sugar and fat diets, synergizes with aging to drive tissue dysfunction. Old mice on a short-term high sugar diet show cardiac hypertrophy which is attenuated by elamipretide (otherwise known as SS-31, a small peptide that modifies mitochondrial function) treatment [ 4 , 32 ]. Surprisingly, a high fat diet is protective against age-associated skeletal muscle sarcopenia and promotes fatigue resistance.…”

Section: Session One: Organ Aging and Growth Signalingmentioning

confidence: 99%

Proceedings from the annual University of Washington Geroscience Symposium, October 23, 2020

2021

Self Cite

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The University of Washington Nathan Shock Center of Excellence in the Biology of Aging in conjunction with the Healthy Aging and Longevity Research Institute held its annual geroscience symposium virtually on October 23, 2020. The symposium was divided into three sessions: (I) organ aging and growth signaling, (II) neurodegeneration and metabolism, and (III) innovative approaches in geroscience and aging research. Nine speakers affiliated with the University of Washington and three invited guest speakers, predominantly trainee, and junior faculty presented their research. Here, we summarize research presented during the symposium. A geroscience special issue, of which this is a part, collects submissions from symposium presenters as well as trainees supported by the Biological Mechanisms of Healthy Aging training program.

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SS‐31 and NMN: Two paths to improve metabolism and function in aged hearts

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 45 publications

References 45 publications

Hypertension-induced cognitive impairment: from pathophysiology to public health

Hypertension-induced cognitive impairment: from pathophysiology to public health

Mitochondrial dysfunction and potential mitochondrial protectant treatments in tendinopathy

Proceedings from the annual University of Washington Geroscience Symposium, October 23, 2020

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