Targeting phospholipase

Sanne van der Rijt, Simone W Denis, Loes M Butter, Bauke V Schomakers, Rob Ofman, Michel van Weeghel, Frédéric M Vaz, Adrie D Dane, Sander R Piersma, Connie R Jimenez, Sandrine Florquin, Arwen W Gao, Georges E Janssens, Riekelt H Houtkooper, Alessandra Tammaro

Laboratory Genetic Metabolic Diseases, Department of Laboratory Medicine, Amsterdam UMC location University of Amsterdam, Amsterdam 1105 AZ, The Netherlands.Laboratory Genetic Metabolic Diseases, Department of Laboratory Medicine, Amsterdam UMC location University of Amsterdam, Amsterdam 1105 AZ, The Netherlands. · pubmed

Paper

Abstract

Chronic kidney disease (CKD), a major age-related pathology, is driven by the accumulation of chronic senescent proximal tubular epithelial cells (TECs), promoting fibrosis and functional decline. Although senescence involves metabolic reprogramming, the role of complex lipid metabolism in TECs senescence remains poorly understood. Here, we identify a critical role for lysosomal phospholipid metabolism in senescent TECs. We show that the lysosomal phospholipid bis(monoacylglycerol)phosphate (BMP) increases during kidney aging and in senescent TECs. Genetic knockout of the BMP hydrolase

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Research summary

The paper claims that lysosomal phospholipid bis(monoacylglycerol)phosphate (BMP) accumulates in senescent proximal tubular epithelial cells and drives chronic kidney disease progression. This is relevant because it identifies a specific metabolic mechanism underlying cellular senescence, a fundamental driver of aging, rather than merely treating the downstream symptoms of kidney failure.

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