Articles

This study describes that cardiolipin deficiency-induced mitochondrial dysfunction in T_reg cells impairs gut–immune tolerance.

This study describes a novel mechanism of calcium control of metabolism found in the mitochondrial intermembrane space that is entirely independent of matrix Ca²⁺ uptake.

Metformin is shown to exert its glucose-lowering and additional clinical effects through inhibition of mitochondrial complex I in the intestinal epithelium in mice.

Faecal microbiome profiling of individuals with obesity and type 2 diabetes (T2D) before and 12 months after bariatric surgery links surgery-induced changes in microbiota composition to metabolic improvements and potentially to T2D remission.

Succinate acts as a competitive inhibitor of mammalian aspartate transcarbamylase (ATCase), leading to impaired pyrimidine biosynthesis and reduced proliferation under SDH inhibition.

This study develops a platform that enables simultaneous, multiplexed tracing of 30 nitrogen isotope-labelled metabolites, uncovering differences in pyrimidine synthesis pathway choice between primitive and differentiated cells.

Bile acids are shown to control biliary epithelial cell identity and function via FXR–YAP signalling, maintaining biliary integrity and tissue homeostasis in the context of liver fibrosis.

Tissue-specific fibroblast lipid cues are shown to significantly influence the invasion rate of squamous cell carcinomas (SCCs), with oral and lung fibroblasts promoting aggressive cancer behaviour through distinct lipid metabolic pathways, while dermal fibroblasts, being lipid poor, limit cutaneous SCC invasion.

Beta-adrenergic signalling modulates histone variant H2A.Z deposition, chromatin accessibility and chromatin loop reorganization to regulate thermogenesis in mouse and human adipocytes.

This study reveals that tissue redox rhythms are altered in ageing mice but can be restored through time-restricted application of antioxidants or pro-oxidants, leading to improved physiological functions and ameliorated ageing-related impairments.

In a multi-cohort longitudinal study integrating continuous glucose monitoring and circulating proteomics, cumulative age-related disease trajectories shape daily glycaemic variability and postprandial response to standardized meals.

This study demonstrates that overexpression of irisin, an exercise-induced myokine, ameliorates obesity and insulin resistance in high-fat-diet-fed mice by increasing local IL-33 production and preserving ST2⁺ regulatory T cells in white adipose tissues.

ROS-mediated sulfenylation or ‘oxidative activation’ of p-GSK-3β can terminate glycogenesis and initiate gluconeogenesis by modulating Gys2 and FoxO1, leading to hepatic insulin resistance.

Using single-cell tissue imaging and spatial proteomics to study mitochondria–lipid droplet coupling in hepatocytes, PLIN5 phosphorylation is identified as a mediator of lipid flux and nutrient stress responses.

DGAT1 controls sex-specific CD8⁺ T cell responses in tumours, reducing mitochondrial function and tumour control in female mice, but protecting against oxidative stress and tumour growth in male mice through androgen receptor signalling.

The accumulation of phosphoinositides at the lysosomal surface is shown to enhance RagGTPase–mTORC1 activity, which affects skeletal muscle cell differentiation. Inhibition of this signalling pathway improves muscle physiology in a mouse myopathy model.

A distinct lipid-laden subset of monocyte-derived macrophages regulates hepatocyte proliferation and liver regeneration in injured livers, via CD36-mediated signalling.

Tanycyte-derived extracellular vesicles are shown to regulate feeding diurnality and metabolic balance through insulin precursor-mediated targeting and delivery of mTORC components to hypothalamic neurons.

TRIP6 phosphorylation triggers a signalling cascade that promotes glycolysis in KRAS-mutant colorectal cancer cells. The resulting lactate accumulation drives extracellular lactylation of CD44 on CD8⁺ T cells, thereby compromising their anti-tumour activity.

ECM1, a key mediator of extracellular matrix–mitochondrial crosstalk, modulates mitochondrial function through a mechano-metabolic pathway to mediate kidney fibrosis.