Aspirin Inhibits Oxidant Stress, Reduces Age-Associated Functional Declines, and Extends Lifespan of <i>Caenorhabditis elegans</i>

Ayyadevara, Srinivas; Bharill, Puneet; Dandapat, Abhijit; Hu, Chong; Khaidakov, Magomed; Mitra, Sona; Reis, Robert J. Shmookler; Mehta, Jawahar L.

doi:10.1089/ars.2011.4151

Cited by 103 publications

(105 citation statements)

References 49 publications

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“…We first investigated the role of the insulin signaling pathway, which is known to regulate lifespan in multiple species (Kenyon, 2010). Similar to previous results using other salicylic acid derivatives (Ayyadevara et al, 2013; Wan et al, 2013), worms defective for the insulin signaling pathway, daf‐16(mu86) mutants, were unresponsive to C8‐SA. Indeed, daf‐16(mu86) mutants harbored similar mean and maximal lifespan when exposed to C8‐SA or the vehicle (Figure 2a and Table 1).…”

Section: Resultssupporting

confidence: 88%

“…This compound shows similar effects in C. elegans to other salicylic acid derivatives published earlier such as ASA and salicylic acid itself (Ayyadevara et al, 2013; Wan et al, 2013). Worms exposed to C8‐SA lived on average 19% longer than untreated controls (Figure 1a and Table 1) and remained healthier for longer periods of time.…”

Section: Resultssupporting

confidence: 76%

“…It is important to note that there have been earlier reports showing that both acetylsalicylic and salicylic acids could extend C. elegans ’ lifespan (Ayyadevara et al, 2013; Wan et al, 2013). In these reports, several genes were shown to be important for the lifespan effect of these compounds, including the AMPK, the forkhead transcription factor DAF‐16/FOXO and other genes involved in the oxidative stress response.…”

Section: Discussionmentioning

confidence: 96%

“…AMPK has also been suggested to control the aging process in general (Salminen & Kaarniranta, 2012), and targeting AMPK has been discussed as a potential strategy to slow down aging in humans (Longo et al, 2015). Interestingly, ASA has recently been revealed as a lifespan‐extending treatment in both mice and nematodes (Ayyadevara et al, 2013; Strong et al, 2008; Wan, Zheng, Wu, & Luo, 2013). Salicylic acid also extends lifespan of C. elegans, albeit with a less pronounced effect than ASA (Ayyadevara et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…Interestingly, ASA has recently been revealed as a lifespan‐extending treatment in both mice and nematodes (Ayyadevara et al, 2013; Strong et al, 2008; Wan, Zheng, Wu, & Luo, 2013). Salicylic acid also extends lifespan of C. elegans, albeit with a less pronounced effect than ASA (Ayyadevara et al, 2013). Work on the molecular mechanism in C. elegans has shown that activation of AAK‐2/AMPK and DAF‐16/FOXO was required for the lifespan‐extending activity of ASA (Wan et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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A salicylic acid derivative extends the lifespan of Caenorhabditis elegans by activating autophagy and the mitochondrial unfolded protein response

et al. 2018

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Plant extracts containing salicylates are probably the most ancient remedies to reduce fever and ease aches of all kind. Recently, it has been shown that salicylates activate adenosine monophosphate‐activated kinase (AMPK), which is now considered as a promising target to slow down aging and prevent age‐related diseases in humans. Beneficial effects of AMPK activation on lifespan have been discovered in the model organism Caenorhabditis elegans (C. elegans). Indeed, salicylic acid and acetylsalicylic acid extend lifespan in worms by activating AMPK and the forkhead transcription factor DAF‐16/FOXO. Here, we investigated whether another salicylic acid derivative 5‐octanoyl salicylic acid (C8‐SA), developed as a controlled skin exfoliating ingredient, had similar properties using C. elegans as a model. We show that C8‐SA increases lifespan of C. elegans and that a variety of pathways and genes are required for C8‐SA‐mediated lifespan extension. C8‐SA activates AMPK and inhibits TOR both in nematodes and in primary human keratinocytes. We also show that C8‐SA can induce both autophagy and the mitochondrial unfolded protein response (UPRmit) in nematodes. This induction of both processes is fully required for lifespan extension in the worm. In addition, we found that the activation of autophagy by C8‐SA fails to occur in worms with compromised UPRmit, suggesting a mechanistic link between these two processes. Mutants that are defective in the mitochondrial unfolded protein response exhibit constitutive high autophagy levels. Taken together, these data therefore suggest that C8‐SA positively impacts longevity in worms through induction of autophagy and the UPRmit.

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Section: Resultssupporting

confidence: 88%

Section: Resultssupporting

confidence: 76%

Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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A salicylic acid derivative extends the lifespan of Caenorhabditis elegans by activating autophagy and the mitochondrial unfolded protein response

et al. 2018

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Reactive Oxygen Species Scavenging Nanomedicine for the Treatment of Ischemic Heart Disease

Zhang

Dalan

et al. 2022

Advanced Materials

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Ischemic heart disease (IHD) is the leading cause of disability and mortality worldwide. Reactive oxygen species (ROS) have been shown to play key roles in the progression of diabetes, hypertension, and hypercholesterolemia, which are independent risk factors that lead to atherosclerosis and the development of IHD. Engineered biomaterial‐based nanomedicines are under extensive investigation and exploration, serving as smart and multifunctional nanocarriers for synergistic therapeutic effect. Capitalizing on cell/molecule‐targeting drug delivery, nanomedicines present enhanced specificity and safety with favorable pharmacokinetics and pharmacodynamics. Herein, the roles of ROS in both IHD and its risk factors are discussed, highlighting cardiovascular medications that have antioxidant properties, and summarizing the advantages, properties, and recent achievements of nanomedicines that have ROS scavenging capacity for the treatment of diabetes, hypertension, hypercholesterolemia, atherosclerosis, ischemia/reperfusion, and myocardial infarction. Finally, the current challenges of nanomedicines for ROS‐scavenging treatment of IHD and possible future directions are discussed from a clinical perspective.

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We are all aging, and here's why

et al. 2022

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Aging, in simple words, is the gradual decline of an individual organism's health and vitality. Aging, as of yet, is the inevitable side effect of the body's normal functioning. Aging, arguably the most complex human phenotype, is the combined effect of all processes in an organism that leads to a probabilistic increase in the occurrence of disease and eventually death. The characteristics of aging are its complexity and its late-life multimorbidity. The enormous complexity of the aging process is attributed to the large number of interconnected networks of pathways that influence the aging phenotype.Because aging occurs throughout the body of an organism, it leads to a combined loss of efficiency in conventional organ/tissue, such as breakdown of tissue integrity, stem cell dysfunction, and cancer, leading to multimorbidity.So far, research has identified a few independent root causes responsible for the widespread effects of aging and age-associated disease, which comprise cell death or senescence; rapidly dividing cells; cells resistant to death; mitochondrial dysfunction; accumulation of extracellular toxic substances; molecules leading to DNA damage such as oxidizing species (ROS and RNS); and loss of stem cells. The effect of aging and the occurrence of aging-associated diseases in an organism can be considerably brought down by targeting these basic causes.Our body has its own aging mechanism working at a different magnitude, therefore giving a differential contribution to the phenotype of aging. Hence, there is a promising future for personalized medicine to enter and affect the field of aging. Every person can be predisposed to having a higher rate of aging in one system than another (for example, the heart, liver, metabolic system, and immune system).

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Aspirin Inhibits Oxidant Stress, Reduces Age-Associated Functional Declines, and Extends Lifespan of Caenorhabditis elegans

Cited by 103 publications

References 49 publications

A salicylic acid derivative extends the lifespan of Caenorhabditis elegans by activating autophagy and the mitochondrial unfolded protein response

A salicylic acid derivative extends the lifespan of Caenorhabditis elegans by activating autophagy and the mitochondrial unfolded protein response

Reactive Oxygen Species Scavenging Nanomedicine for the Treatment of Ischemic Heart Disease

We are all aging, and here's why

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