We are analyzing https://link.springer.com/article/10.1007/s10522-023-10040-3.

Title:
Dynamics of redox signaling in aging via autophagy, inflammation, and senescence | Biogerontology
Description:
Review paper attempts to explain the dynamic aspects of redox signaling in aging through autophagy, inflammation, and senescence. It begins with ROS source in the cell, then states redox signaling in autophagy, and regulation of autophagy in aging. Next, we discuss inflammation and redox signaling with various pathways involved: NOX pathway, ROS production via TNF-α, IL-1β, xanthine oxidase pathway, COX pathway, and myeloperoxidase pathway. Also, we emphasize oxidative damage as an aging marker and the contribution of pathophysiological factors to aging. In senescence-associated secretory phenotypes, we link ROS with senescence, aging disorders. Relevant crosstalk between autophagy, inflammation, and senescence using a balanced ROS level might reduce age-related disorders. Transducing the context-dependent signal communication among these three processes at high spatiotemporal resolution demands other tools like multi-omics aging biomarkers, artificial intelligence, machine learning, and deep learning. The bewildering advancement of technology in the above areas might progress age-related disorders diagnostics with precision and accuracy.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

pubmed, article, google, scholar, cas, central, aging, cell, redox, autophagy, signaling, senescence, oxidative, biol, stress, role, sci, ageing, human, httpsdoiorgs, cells, med, oxygen, reactive, cellular, rev, disease, nat, nature, httpsdoiorg, ros, damage, inflammation, signal, diseases, species, regulation, pathway, myeloperoxidase, senescenceassociated, activation, nox, oxidase, secretory, biomarkers, acad, springer, senescent, free, biochem,

Topics {✒️}

camp-pka-ampk-nf-κb axis ros-activated nf-κb signalling cell surface-bound il-1alpha month download article/chapter sqstm1/p62 activates nfe2l2/nrf2 activation-induced t-cell death thiol-based cell signalling epithelial–mesenchymal transition induced drug-induced cellular senescence ai-driven longevity research context-dependent signal communication double-edged sword revisited pink1/parkin‐mediated mitophagy kavitha thirumurugan ros-generating nadph oxidases reduce age-related disorders full article pdf senescence regulator interleukin-1α il-6/il-8 cytokine network ros-generating oxidases nox1 passos jf age-related nad+ decline mouse cells dependent article biogerontology aims reactive oxygen production nf-κb activation nrf2-p62 autophagy pathway reactive oxygen species superoxide-mediated redox signaling camp/ampk signaling nauseef wm p53 tumor suppressor atayik mc kt formed fig mitochondria-targeted senotherapeutic interventions gp91phox expression induced neutrophil respiratory burst cellular signal transduction ras-dependent signaling privacy choices/manage cookies ros-dependent manner senescence-induced senescence human telomere biology orjalo av pham-huy secreted protein igfbp7 multi-omics aging biomarkers proc biol sci age-dependent decline pearl research park

Questions {❓}

Azzi A (2022) Oxidative stress: what is it?
Birch J, Passos JF (2017) Targeting the SASP to combat ageing: mitochondria as possible intracellular allies?
Emanuele E, Minoretti P, Sanchis-Gomar F et al (2014) Can enhanced autophagy be associated with human longevity?
Kirkwood TBL, Austad SN (2000) Why do we age?

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