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Loss of muscle satellite cells during aging has been thought to contribute to sarcopenia, but experimentally induced depletion of these cells in adult mice does not result in this condition.
Alternative splicing of the gene encoding VEGF-A under ischemic conditions generates an antiangiogenic isoform of the protein that impairs revascularization under conditions of metabolic dysfunction in mice, and this isoform is found at elevated levels in patients with peripheral artery disease.
Two papers in this issue, by Bruns et al. and Zhao et al., show that megakaryocytes constitute a niche for hematopoietic stem cells in the mouse bone marrow and produce factors that regulate hematopoietic stem cell quiescence and proliferation.
Two papers in this issue, by Bruns et al. and Zhao et al., show that megakaryocytes constitute a niche for hematopoietic stem cells in the mouse bone marrow and produce factors that regulate hematopoietic stem cell quiescence and proliferation.
TH17 and Treg cell development are reciprocally regulated by de novo fatty acid synthesis, and inhibition of acetyl-CoA carboxylase 1 (ACC1) attenuates TH17 cell–mediated autoimmune disease.
Elevated plasma levels of branched chain amino acids detected prior to pancreatic cancer diagnosis may result from whole body tissue breakdown occurring during the early stages of this disease.
Gibbons et al. show that T cells in newborns, previously thought to have a limited ability to fight infection, can produce interleukin-8, an effector of innate immunity.
Genetic deletion of the lysosomal Ca2+ channel MCOLN1 in mice results in muscular dystrophy, implicating this source of calcium in muscle membrane repair.
Rampias et al. report that inactivating mutations in Notch pathway components are frequent in human bladder cancer and drive bladder tumorigenesis in mice.
Cytotoxic T cells are necessary and sufficient for the development of alopecia areata in mice, while JAK inhibition promotes regrowth of hair in patients and mice with established disease.