2 research outputs found

    Modeling Renal Disease “On the Fly”

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    Detoxification is a fundamental function for all living organisms that need to excrete catabolites and toxins to maintain homeostasis. Kidneys are major organs of detoxification that maintain water and electrolyte balance to preserve physiological functions of vertebrates. In insects, the renal function is carried out by Malpighian tubules and nephrocytes. Due to differences in their circulation, the renal systems of mammalians and insects differ in their functional modalities, yet carry out similar biochemical and physiological functions and share extensive genetic and molecular similarities. Evolutionary conservation can be leveraged to model specific aspects of the complex mammalian kidney function in the genetic powerhouse Drosophila melanogaster to study how genes interact in diseased states. Here, we compare the human and Drosophila renal systems and present selected fly disease models

    The Biology of Vasopressin

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    Vasopressins are evolutionarily conserved peptide hormones. Mammalian vasopressin functions systemically as an antidiuretic and regulator of blood and cardiac flow essential for adapting to terrestrial environments. Moreover, vasopressin acts centrally as a neurohormone involved in social and parental behavior and stress response. Vasopressin synthesis in several cell types, storage in intracellular vesicles, and release in response to physiological stimuli are highly regulated and mediated by three distinct G protein coupled receptors. Other receptors may bind or cross-bind vasopressin. Vasopressin is regulated spatially and temporally through transcriptional and post-transcriptional mechanisms, sex, tissue, and cell-specific receptor expression. Anomalies of vasopressin signaling have been observed in polycystic kidney disease, chronic heart failure, and neuropsychiatric conditions. Growing knowledge of the central biological roles of vasopressin has enabled pharmacological advances to treat these conditions by targeting defective systemic or central pathways utilizing specific agonists and antagonists
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