Kynurenine pathway dysregulation via loss of QPRT drives declines in activity and altered metabolism in mice.

Reyhan Westbrook, Vinal Menon, Joy Cagmat, Timothy Garrett, Robert Schwarcz, Jeremy Walston, Peter M Abadir, Tae Chung

Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. [email protected]. · pubmed

Paper

Abstract

Chronic inflammatory pathway activation increases with age and is epidemiologically linked to multiple aging-related pathophysiological processes, phenotypes such as physical frailty and sarcopenia and early healthspan declines in aging organisms. Despite this, molecular mechanisms that directly connect chronic inflammation to these conditions remain poorly characterized. We hypothesize that chronic inflammation contributes to the development of age-related phenotypes by increasing the degradation of dietary tryptophan into multiple metabolites with unique physiological properties, called kynurenines, via the 'kynurenine pathway' (KP). To understand the impact of elevated KP metabolites on mammalian healthspan we utilized the quinolinate phosphoribosyltransferase knock-out (QPRT

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Research summary

Chronic inflammation drives the degradation of dietary tryptophan into kynurenines, impacting healthspan in aging organisms. The study addresses the molecular mechanisms linking chronic inflammation to age-related phenotypes, which is crucial for understanding and potentially mitigating the root causes of aging.

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