{'fraction_non_alphanumeric': 0.029265599116510214, 'fraction_numerical': 0.018774157923799006, 'mean_word_length': 5.4714285714285715, '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}}
Dual role of microsomal prostaglandin E synthase 1 in chronic kidney disease.

See related article, pp 122–128

Chronic kidney disease (CKD) is typically thought of as a progressive loss of glomerular filtration rate. However, CKD is also a systemic disorder in which loss of glomerular filtration rate or functional renal mass leads to dysregulation of extracellular fluid and electrolyte balance, impaired bone and mineral metabolism, and hematologic abnormalities, such as anemia and platelet dysfunction.1 Identification of biological mediators that reduce progressive renal injury and attenuate anemia of chronic renal failure is a crucial step in developing treatments for the 26 million people with CKD in the United States.1

Prostanoids are the subject of intense interest as potential therapeutic targets in renal disease because of their critical roles in regulation of blood pressure, renal blood flow, glomerular filtration rate, and inflammation.2,3 Individual prostanoids are derived from the metabolism of arachidonic acid by the sequential actions of cyclooxygenase (COX) and specific prostanoid synthases.2 In addition to COX activity, the biological effects of prostanoids are dependent on a number of other factors, including the tissue distribution and expression of individual prostanoid synthases and prostanoids receptors.2 The most abundant prostanoid in the kidney, prostaglandin E2 (PGE2), is produced by 3 isoforms of prostaglandin E synthase (PGES): membrane PGES-1 (mPGES-1), mPGES-2, and cytosolic PGES.2,3 The biological effects of PGE2 are mediated by activation of 4 receptor subtypes (EP1, EP2, EP3, and EP4). Like COX-2, the expression of mPGES-1 increases in response to inflammatory stimuli, and mPGES-1 is functionally coupled and colocalized with COX.3,4 Recent studies …