Developmental ROS individualizes organismal stress resistance and lifespan

Bazopoulou, Daphne; Knoefler, Daniela; Zheng, Yongxin; Ulrich, Kathrin; Oleson, Bryndon J.; Xie, Lihan; Kim, Minwook; Kaufmann, Anke; Lee, Young Tae; Dou, Yali; Chen, Yong; Qin, Shu; Jakob, Ursula

doi:10.1038/s41586-019-1814-y

Cited by 182 publications

(159 citation statements)

References 36 publications

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“…An indication of the need for subtlety in thinking about the relation of ROS to ageing and lifespan comes from the finding by Bazopoulou et al [ 307 ] that a transient (10 h) increase in ROS in early development of Caenorhabditis triggers epigenetic mechanisms that result in increased stress resistance and redox homeostasis that in turn result in life span extension, the mediating mechanism being global decreases in histone H3K4me3 levels. A biphasic response such as this, where low levels of a potentially damaging molecule which is toxic at higher doses triggers the upregulation of cellular defense mechanisms that are ultimately beneficial to life expectancy was termed mitohormesis by Tapia [ 308 ].…”

Section: Mitochondrial Mutations and The Oxidative Damage Theorymentioning

confidence: 99%

Intimate Relations—Mitochondria and Ageing

Webb¹,

Sideris²

2020

IJMS

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Mitochondrial dysfunction is associated with ageing, but the detailed causal relationship between the two is still unclear. We review the major phenomenological manifestations of mitochondrial age-related dysfunction including biochemical, regulatory and energetic features. We conclude that the complexity of these processes and their inter-relationships are still not fully understood and at this point it seems unlikely that a single linear cause and effect relationship between any specific aspect of mitochondrial biology and ageing can be established in either direction.

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Section: Mitochondrial Mutations and The Oxidative Damage Theorymentioning

confidence: 99%

Intimate Relations—Mitochondria and Ageing

Webb¹,

Sideris²

2020

IJMS

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“…For example, Murphy's group [112] used mPEG to show that mitochondrial reactive species inactivate pyruvate dehydrogenase kinase 2. Recently, Jakob's group [113] demonstrated that histone methyltransferase oxidation, evidenced using mPEG, decreases methylation, which enables stochastic fluxes in developmental reactive species to regulate lifespan via an epigenetic switch. The utility of mPEG is, however, limited because the bulky PEG sterically impedes thiol labelling [98].…”

Section: Click Pegylationmentioning

confidence: 99%

Immunological Techniques to Assess Protein Thiol Redox State: Opportunities, Challenges and Solutions

Cobley

Husi

2020

Antioxidants

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To understand oxidative stress, antioxidant defense, and redox signaling in health and disease it is essential to assess protein thiol redox state. Protein thiol redox state is seldom assessed immunologically because of the inability to distinguish reduced and reversibly oxidized thiols by Western blotting. An underappreciated opportunity exists to use Click PEGylation to realize the transformative power of simple, time and cost-efficient immunological techniques. Click PEGylation harnesses selective, bio-orthogonal Click chemistry to separate reduced and reversibly oxidized thiols by selectively ligating a low molecular weight polyethylene glycol moiety to the redox state of interest. The resultant ability to disambiguate reduced and reversibly oxidized species by Western blotting enables Click PEGylation to assess protein thiol redox state. In the present review, to enable investigators to effectively harness immunological techniques to assess protein thiol redox state we critique the chemistry, promise and challenges of Click PEGylation.

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“…to induce and regulate a complex signaling network between mitochondria, the nucleus (Quiros et al, 2016), other organelles, such as lysosomes (Ramachandran et al, 2019), and the cytosol (D'Amico et al, 2017), resulting in increased cell stress resistance that can improve health and extend lifespan. Of particular interest is the recent observation that early developmental transient redox stress in Caenorhabditis elegans could indeed modify the methylation state of the genome, and lead to increased stress resistance, improved redox homeostasis, and prolonged lifespan (Bazopoulou et al, 2019).…”

Section: Ros and Mitochondria In Aging Progressionmentioning

confidence: 99%

Do You Remember Mitochondria?

2020

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Dementia is one among the consequences of aging, and amnesia is often one of the most common symptoms. The lack of memory, as a consequence of both "healthy" aging or neurodegenerative conditions, such as in Alzheimer's disease, has a dramatic impact on the patient's lifestyle. In fact, the inability to recall information made by a previous experience could not only alter the interaction with the environment, but also lead to a loss of identity. Mitochondria are key regulators of brain's activity; thanks to their "dynamic organelles" nature they constantly rearrange in the cell body and move along axons and dendrites, changing in dimension, shape, and location, accordingly to the cell's energy requirements. Indeed, the energy they can provide is essential to maintain synaptic plasticity and to ensure transmission through presynaptic terminals and postsynaptic spines. Stressful conditions, like the ones found in neurodegenerative diseases, seriously impair mitochondria bioenergetic, leading to both loss of proper neuronal interaction and of neuron themselves. Here, we highlighted the current knowledge about the role of mitochondria and mitochondrial dynamics in relation to neurodegenerative disorders linked to aging. Furthermore, we discuss the obstacles as well as the future perspectives aimed to enlarge our knowledge about mitochondria as target for new therapeutic strategies to slow down aging and neurodegenerative disease's symptoms.

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Developmental ROS individualizes organismal stress resistance and lifespan

Cited by 182 publications

References 36 publications

Intimate Relations—Mitochondria and Ageing

Intimate Relations—Mitochondria and Ageing

Immunological Techniques to Assess Protein Thiol Redox State: Opportunities, Challenges and Solutions

Do You Remember Mitochondria?

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