{'fraction_non_alphanumeric': 0.03987068965517242, 'fraction_numerical': 0.03017241379310345, 'mean_word_length': 5.635714285714286, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Xenobiotic export pumps, endothelin signaling, and tubular nephrotoxicants—a case of molecular hijacking

This article is a review on recent studies in intact renal proximal tubules that link tubular nephrotoxicants with endothelin (ET) regulation of xenobiotic export pump function. The data show that transport on p‐glycoprotein and Mrp2 decreases rapidly when ET signals through an ETB receptor, NO synthase (NOS), and protein kinase C (PKC). Surprisingly, nephrotoxicants, such as radiocontrast agents, aminoglycoside antibiotics, and heavy metal salts, “hijack” this signaling pathway, causing ET release from the tubules, hormone binding to its receptor, activation of NOS and PKC, and reduced xenobiotic transport. These findings suggest a new common mechanism by which nephrotoxicants may act to disrupt renal tubular function. © 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol 16:121–127, 2002. DOI 10.1002/jbt.10030