from: https://pubmed.ncbi.nlm.nih.gov/30072093/Abstract
Mitohormesis is a term used to define a biological response where the induction of a reduced amount of mitochondrial stress leads to an increment in health and viability within a cell, tissue, or organism. The mitochondrial stress response activated by a potentially damaging stimulus requires a coordinated dialogue with the cellular nucleus, known as mitonuclear communication. This interplay induced by the hormetic response in mitochondria relies in a variety of signals among which the most relevant ones are reactive oxygen species (ROS), mitochondrial metabolites, proteotoxic signals, the mitochondria-cytosol stress response, and the release of mitokines. The activation of the mitohormetic response increases lifespan in different animal models, from worms to mammals. Further, mitohormesis also enhances healthspan, particularly improving metabolism and immune system. Although multiple mediators and stress signals have been proposed to activate this protective mechanism, beneficial outcomes of mitohormesis are most probably due to an increase in mitochondrial ROS. Activation of other protective stress mechanisms as mitochondrial unfolded protein response or the increase in the expression of mitokines are also associated with the positive benefits exerted by mitohormesis. Herein, we review the different mitohormetic signals and pathways described from worms to mammals and their effects on health and survival. The identification and description of pathways and molecules implicated in the beneficial effects of mitohormesis will help understand the complex balance between death and survival in the face of mitochondrial damage and will allow to open a novel area of therapies aimed at improving health in humans.
from: https://www.news-medical.net/life-sciences/What-is-Mitohormesis.aspxWhat is Mitohormesis?
Mitochondria are important cellular organelles that act as the cellular ‘power house’. Mitochondria generate ATP as a source of energy through a process called oxidative phosphorylation. During this process, mitochondria also produce ROS as by-products. In the initial years of discovery, ROS were believed to have only harmful effects in term of inducing oxidative damages to various cellular components, including proteins, lipids, and DNA.
However, recent scientific evidence has clearly indicated that ROS can also be beneficial for the cells. In response to mild cellular stress, mitochondria generate low levels of ROS, which in turn act as signaling molecules and protect the cells from further damage by initiating an adaptive response (stress defense mechanism). This process is known as mitochondrial hormesis or mitohormesis.
that's part of the discovery here:Mitochondrial processes definitely aren't as simple as "ROS bad". Simplistic theory would claim that peroxynitrite scavengers are good for you, but for me, they make my ME symptoms worse.
maybe that's what's not working in PwME, the threshold for "mild cellular stress" might be nonexistent or at least drastically lowered, so those positive effects never occur. and a failure with the mitochondrial adaptive stress defense response sounds like it could explain exercise intolerance and maybe even PEM.ROS can also be beneficial for the cells
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ROS, which in turn act as signaling molecules and protect the cells from further damage by initiating an adaptive response (stress defense mechanism)
While I hadn't read anything specific about it, I just accepted that the various interactions in the mitochondria are very complex, so unless someone discovered a specific abnormality in PWME, it's not really worth speculating about.i was surprised i've never seen it even being discussed.
