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Healthspan pathway maps in C. elegans and humans highlight transcription, proliferation/biosynthesis and lipids.

PMID: 32634117 (view PubMed database entry)
DOI: 10.18632/aging.103514 (read at publisher's website )
PMCID: PMC7377848 (free full text version available)

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Steffen Möller, Nadine Saul, Alan A Cohen, Rüdiger Köhling, Sina Sender, Hugo Murua Escobar, Christian Junghanss, Francesca Cirulli, Alessandra Berry, Peter Antal, Priit Adler, Jaak Vilo, Michele Boiani, Ludger Jansen, Dirk Repsilber, Hans Jörgen Grabe, Stephan Struckmann, Israel Barrantes, Mohamed Hamed, Brecht Wouters, Liliane Schoofs, Walter Luyten, Georg Fuellen,

The molecular basis of aging and of aging-associated diseases is being unraveled at an increasing pace. An extended healthspan, and not merely an extension of lifespan, has become the aim of medical practice. Here, we define health based on the absence of diseases and dysfunctions. Based on an extensive review of the literature, in particular for humans and C. elegans, we compile a list of features of health and of the genes associated with them. These genes may or may not be associated with survival/lifespan. In turn, survival/lifespan genes that are not known to be directly associated with health are not considered. Clusters of these genes based on molecular interaction data give rise to maps of healthspan pathways for humans and for C. elegans. Overlaying healthspan-related gene expression data onto the healthspan pathway maps, we observe the downregulation of (pro-inflammatory) Notch signaling in humans and of proliferation in C. elegans. We identify transcription, proliferation/biosynthesis and lipids as a common theme on the annotation level, and proliferation-related kinases on the gene/protein level. Our literature-based data corpus, including visualization, should be seen as a pilot investigation of the molecular underpinnings of health in two different species. Web address: http://pathways.h2020awe.eu.

Aging (Albany NY) (Aging)
[2020, 12(13):12534-12581]

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