Metabolism
Metabolic dysregulation contributes to the development of dysferlinopathyDysferlin deficiency causes metabolic dysregulation, characterized by mitochondrial abnormalities, death signaling, and elevated glucose uptake and excessive glycogen accumulation in muscle.
Brain and behavioural anomalies caused by Tbx1 haploinsufficiency are corrected by vitamin B12The study shows that mice that are a model of 22q11.2 deletion syndrome have abnormal brain metabolism, and it identifies potential biomarkers of metabolic brain disease in 22q11.2DS patients.
Divergent roles of RIPK3 and MLKL in high-fat diet–induced obesity and MAFLD in miceThis study shows how necroptotic effector MLKL can induce obesity and perturb lipid metabolism to drive MAFLD progression, independent of RIPK3 that regulates inflammatory events.
Mitochondrial apolipoprotein MIC26 is a metabolic rheostat regulating central cellular fuel pathwaysMulti-omics studies combined with functional assays reveal that mitochondrial apolipoprotein MIC26 located in the inner membrane regulates central cellular fuel pathways in a MICOS-independent manner.
NAD+ depletion is central to placental dysfunction in an inflammatory subclass of preeclampsiaInflammatory preeclampsia exhibits a decline in placental NAD+ levels along with mitochondrial impairment, which could be ameliorated by supplementing with NAD+ boosters during pregnancy.
Cholesterol promotes IFNG mRNA expression in CD4+ effector/memory cells by SGK1 activationThe study shows that cholesterol modulates IFNG expression in CD4+ T cells via SGK1 activation, suggesting lipid pathways as potential targets for regulating immune responses in the CNS.
Mitochondria remodeling during endometrial stromal cell decidualizationDecidualization of Endometrial Stromal Cells entails dramatic reshaping of the mitochondrial network, and energetic reshuffling to achieve an efficient secretory phenotype.
Dysfunctional β-cell longevity in diabetes relies on energy conservation and positive epistasisPathologic β-cells become long-lived in diabetes despite high energy conservation based on the control over their metabolic state via PFKFB3 and suppression of Ca2+ toxicity via MAIP1. Inhibition of PFKFB3 eradicates dysfunctional β-cells restoring glucose tolerance in a T2D model.
Reprogramming of breast tumor–associated macrophages with modulation of arginine metabolismA shift of arginine metabolism from polyamine synthesis to nitric oxide synthesis induces reprogramming of macrophages from pro-tumor M2 to anti-tumor M1 types.
Examining the liver–pancreas crosstalk reveals a role for the molybdenum cofactor in β-cell regenerationInvestigation of the inter-organ, pancreas–liver, crosstalk reveals a potential role of the molybdenum biosynthetic pathway in β-cell regeneration.