In vivo imaging reveals that gradually increased amount of glucose mediates the heterogeneous functional development of individual β-cells by activating its major downstream calcineurin/NFAT signaling pathway.
Inhibition of C. elegans FLD-1 or Human TLCD1/2 prevents saturated fat lipotoxicity by allowing increased levels of membrane phospholipids that contain fluidizing long-chain polyunsaturated fatty acids.
Mitophagy regulates mitochondrial quality and mediates extensive mitochondrial degradation in (patho-)physiological settings and is one of the key components of hypoxic preconditioning which protects the heart from ischemia/reperfusion injury.
Pericytes surrounding capillaries in the retina contain α-smooth muscle actin, demonstrating that pericytes have the necessary molecular machinery to change capillary diameter during neurovascular coupling.
Genetic mouse models identify a critical mechanism of myogenic vasoconstriction and reveal the in vivo function of myogenic autoregulation in protecting from organ overperfusion and in maintaining vascular resistance.
Resting-state capillary blood flow and oxygenation are more homogeneous in the deeper cortical layers, underpinning an important mechanism by which the microvascular network adapts to an increased local oxidative metabolism.
The sickle cell trait strongly protects against not only retinopathy-positive cerebral malaria but also retinopathy-negative cerebral malaria, providing evidence that malarial parasites also contribute to retinopathy-negative cerebral malaria and are not innocent bystanders.