How NLRP3 impacts Alzheimer’s disease (AD) is unclear. McManus et al. find that NLRP3 is located at mitochondria where it regulates microglial metabolism. Depletion or chronic pharmacological inhibiti...

How NLRP3 impacts Alzheimer’s disease (AD) is unclear. McManus et al. find that NLRP3 is located at mitochondria where it regulates microglial metabolism. Depletion or chronic pharmacological inhibiti...

MPO activates an immunometabolic rheostat to restrict the functional plasticity of macrophages in favor of proresolving properties.

Glutamine is best known to replenish the TCA cycle through glutaminolysis. Surprisingly, Zhu et al. discover that mitochondrial glutamine import (MGI) functions independently of glutaminolysis in cancer by sustaining Gln-mt-tRNAGln biosynthesis for mitochondrial translation, thus maintaining electron transport chain integrity. Targeting MGI represents a potential strategy to abrogate mitochondrial function in cancer.

New insights into immune cells in the context of neurodegeneration.

Obesity is regarded as a chronic inflammatory disease involving adipose tissue macrophages (ATM), but whether immunometabolic reprogramming of ATM affects obesity remains unclarified. Here we show that in ATM glutaminolysis is the fundamental metabolic flux providing energy and substrate, bridging with AMP-activated protein kinase (AMPK) activity, succinate-induced interleukin-1β (IL-1β) production, and obesity. Abrogation of AMPKα in myeloid cells promotes proinflammatory ATM, impairs thermogenesis and energy expenditure, and aggravates obesity in mice fed with high-fat diet (HFD). Conversely, IL-1β neutralization or myeloid IL-1β abrogation prevents obesity caused by AMPKα deficiency. Mechanistically, ATP generated from glutaminolysis suppresses AMPK to decrease phosphorylation of the β subunit of succinyl-CoA synthetase (SUCLA2), thereby resulting in the activation of succinyl-CoA synthetase and the overproduction of succinate and IL-1β; by contrast, siRNA-mediated SUCLA2 knockdown

Recent evidence highlights the critical role of immune metabolism in the pathogenesis of rheumatoid arthritis (RA). We previously demonstrated that glutaminase 1 (GLS1), a key enzyme in glutamine meta...

The authors provide a comprehensive characterization of how glutamine uptake and utilization regulate macrophage function in atherosclerosis.

Glutamine metabolism is essential for T cell activation and functions. The inhibition of glutaminoly

How NLRP3 impacts Alzheimer’s disease (AD) is unclear. McManus et al. find that NLRP3 is located at mitochondria where it regulates microglial metabolism. Depletion or chronic pharmacological inhibiti...

Cell Death & Disease - LSD1-GLS2 axis drives subtype-specific chemoresistance in pancreatic cancer through glutaminolysis reprogramming

Adipose tissue macrophage (ATM) has been implicated in inflammation and obesity, but the underlying mechanisms are still unclear. Here the authors show that AMPK is suppressed in ATMs from mice fed wi...

How NLRP3 impacts Alzheimer’s disease (AD) is unclear. McManus et al. find that NLRP3 is located at mitochondria where it regulates microglial metabolism. Depletion or chronic pharmacological inhibiti...

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Cell Death & Disease - LSD1-GLS2 axis drives subtype-specific chemoresistance in pancreatic cancer through glutaminolysis reprogramming

Glutamine is best known to replenish the TCA cycle through glutaminolysis. Surprisingly, Zhu et al. discover that mitochondrial glutamine import (MGI) functions independently of glutaminolysis in cancer by sustaining Gln-mt-tRNAGln biosynthesis for mitochondrial translation, thus maintaining electron transport chain integrity. Targeting MGI represents a potential strategy to abrogate mitochondrial function in cancer.

How NLRP3 impacts Alzheimer’s disease (AD) is unclear. McManus et al. find that NLRP3 is located at mitochondria where it regulates microglial metabolism. Depletion or chronic pharmacological inhibiti...