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Vascular endothelial growth factor A (VEGF-A) is a potent proangiogenic cytokine elevated in patients with peripheral artery disease (PAD). A new study links impaired vascular regrowth in PAD to increased expression of an antiangiogenic splice variant of VEGF-A.
Diffuse intrinsic pontine glioma is a uniformly lethal malignant tumor of infancy with no effective therapies. A new study reveals that inhibition of JMJD3 has robust antitumor activity in diffuse intrinsic pontine glioma xenografts.
Frontotemporal dementia (FTD) is a neurodegenerative disease that causes social dysfunction and other symptoms. A new study suggests that social dysfunction in FTD is due to decreased microRNA-124 expression and resulting changes in glutamate receptor composition in the prefrontal cortex.
Preosteoclasts give rise to bone-resorbing osteoclasts, which are crucial for skeletal homeostasis. A study now shows that preosteoclasts also contribute to bone formation by releasing platelet-derived growth factor-BB, which promotes bone vascularization and osteogenesis.
Truncation of tau contributes to the formation of neurofibrillary tangles in Alzheimer's disease. A new study finds a direct role for a lysosomal cysteine protease, asparagine endopeptidase, in cleaving tau into neurotoxic fragments.
A recent study reports that de novo fatty acid synthesis is important for differentiation of T helper 17 (TH17) cells. Suppression of this pathway through inhibition of acetyl-CoA carboxylase (ACC) with soraphen A prevents TH17 cell differentiation and consequently enforces a regulatory T cell phenotype.
Mesenchymal stromal cells are key components of hematopoietic stem cell (HSC) niches in the bone marrow. Two studies now show that hematopoietic-derived megakaryocytes also contribute to the HSC niche, regulating HSC quiescence and function.
Increasing evidence points to a role for the immune system in the regulation of metabolism. Two new studies in mice indicate treatment with interleukin-22 restores mucosal immunity in diabetes and alleviates metabolic disease, resulting in improved glycemic control.
A new study shows that plasma levels of branched-chain amino acids are elevated in subjects several years before they are diagnosed with pancreatic cancer. This may reflect breakdown of peripheral protein stores in the early stages of the disease.
Altered stem cell homeostasis underlies functional tissue decline during muscle aging and disease progression. Janus kinase–signal transducer and activator of transcription (JAK-STAT) signal transduction is a crucial regulator of muscle regeneration, and targeting this pathway in mice relieves aspects of debilitating muscle wasting.
A new study identifies recurrent somatic duplications of a NOTCH1-driven enhancer of MYC in human T cell leukemia. This enhancer is required for both normal and malignant T cell development.
Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system. A new study has shown that the lipid lactosylceramide, produced by astrocytes, contributes to disease progression in a mouse model of MS.
Alzheimer's disease is characterized by severe cognitive decline and brain amyloid plaques. A new study in mouse models that develop features of Alzheimer's disease indicates that progranulin may have a role in clearing these plaques.
Disrupted differentiation of Schwann cells contributes to axonal loss in a rat model of Charcot-Marie-Tooth 1A neuropathy. Early neuregulin-1 treatment promotes Schwann cell differentiation, preserves axons and restores nerve function in this model.
Aging and a high-fat diet are predisposing factors for type 2 diabetes. A study in mice suggests that dietary fat and aging lead to atypical transforming growth factor-β1 signaling in the hypothalamus, which disturbs whole-body glucose regulation.
Mutations in the DMD gene, encoding dystrophin, cause the most common forms of muscular dystrophy. A new study shows that forcing translation of DMD from an internal ribosome entry site can alleviate Duchenne muscular dystrophy symptoms in a mouse model.
Alopecia areata is an immune-mediated, nonscarring form of hair loss. A new study using human clinical samples and a mouse model demonstrates that CD8αβ+NKG2D+ T effector memory cells mediate alopecia areata in part through Janus kinase (JAK) signaling and that alopecia areata might be treated with JAK inhibitors.
Inflammatory diseases typically display circadian variation in symptom severity. A new study in mice shows how a pulmonary epithelial cell clock controls neutrophil recruitment to the lungs and provides insight into interactions between local and systemic circadian clocks.
Restriction factors are host cell proteins that inhibit retroviral infection. A new study using mutants of human HIV-1 restriction factor SAMHD1 suggests that it inhibits infection through degradation of viral RNA rather than through its dNTPase activity as previously suggested.
