Ageing is characterized by progressive metabolic and inflammatory dysregulation, in which methylglyoxal (MGO), a highly reactive dicarbonyl by-product of glycolysis, is involved in the formation of advanced glycation end products (AGEs). This review provides an integrated overview of the bidirectional relationship between MGO-derived carbonyl stress and the gut microbiota, focusing on its implications for ageing and age-related diseases. We summarize current evidence on MGO production, clearance, tissue distribution, and reactivity, with particular attention to the intestinal lumen as a site where dietary compounds, host metabolism, and microbial activity converge. Age-related dysbiosis may impair intestinal barrier integrity, alter microbial metabolite production, and promote chronic low-grade inflammation, thereby reinforcing metabolic dysfunction and favoring free MGO accumulation. Conversely, MGO and AGEs can reshape microbial communities, compromise epithelial tight junctions, and amplify inflammatory signalling through receptor-dependent and independent mechanisms. Evidence from in vitro, animal, and clinical studies supports a role for the MGO–microbiota axis in metabolic, cardiovascular, gastrointestinal, neurodegenerative, and frailty-related conditions. Targeting microbiota composition, intestinal barrier function, and MGO scavenging pathways may therefore represent a promising strategy to mitigate carbonyl stress and preserve health during ageing.

Microbiota and Methylglyoxal-Derived AGEs: Implications in Ageing and Age-Related Disease / Tombolesi, N., Francini, E., Veronica Badillo-Pazmay, G., Fortunato, C., Marchegiani, F., Olivieri, F., Fumarola, S., Maniscalco, R., Matacchione, G.. - In: LIFE. - ISSN 2075-1729. - 16:8(2026). [10.3390/life16081265]

Microbiota and Methylglyoxal-Derived AGEs: Implications in Ageing and Age-Related Disease

Fabiola Olivieri;
2026-01-01

Abstract

Ageing is characterized by progressive metabolic and inflammatory dysregulation, in which methylglyoxal (MGO), a highly reactive dicarbonyl by-product of glycolysis, is involved in the formation of advanced glycation end products (AGEs). This review provides an integrated overview of the bidirectional relationship between MGO-derived carbonyl stress and the gut microbiota, focusing on its implications for ageing and age-related diseases. We summarize current evidence on MGO production, clearance, tissue distribution, and reactivity, with particular attention to the intestinal lumen as a site where dietary compounds, host metabolism, and microbial activity converge. Age-related dysbiosis may impair intestinal barrier integrity, alter microbial metabolite production, and promote chronic low-grade inflammation, thereby reinforcing metabolic dysfunction and favoring free MGO accumulation. Conversely, MGO and AGEs can reshape microbial communities, compromise epithelial tight junctions, and amplify inflammatory signalling through receptor-dependent and independent mechanisms. Evidence from in vitro, animal, and clinical studies supports a role for the MGO–microbiota axis in metabolic, cardiovascular, gastrointestinal, neurodegenerative, and frailty-related conditions. Targeting microbiota composition, intestinal barrier function, and MGO scavenging pathways may therefore represent a promising strategy to mitigate carbonyl stress and preserve health during ageing.
2026
advanced glycation end products; age-related diseases; ageing; dicarbonyl stress; dysbiosis; glyoxalase system; gut microbiota; inflammaging; intestinal permeability; methylglyoxal
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11566/362121
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