PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23503750-1 2013 BACKGROUND: Urinary plasmin activates the epithelial Na(+) channel (ENaC) in vitro and may possibly be a mechanism of sodium retention in nephrotic syndrome (NS). Sodium 118-124 plasminogen Homo sapiens 20-27 27214087-2 2016 The study was designed to test the hypothesis that the epithelial sodium channel is activated proteolytically by urine plasmin in diabetic nephropathy and mediates renal sodium retention. Sodium 66-72 plasminogen Homo sapiens 119-126 27564657-8 2016 Dermatan sulfate and polyphosphates with sodium as counter ion (Na-PolyP700, Na-PolyP100 and Na-PolyP70) enhanced plasmin-mediated but not thrombin-mediated TAFI activation. Sodium 41-47 plasminogen Homo sapiens 114-121 26933188-2 2016 Recent work has shown stimulation of sodium retention by urinary plasmin during nephrotic syndrome. Sodium 37-43 plasminogen Homo sapiens 65-72 23503750-10 2013 CONCLUSIONS: These findings support the hypothesis that aberrantly filtered plasminogen-plasmin may contribute to ENaC activation and mediate primary renal sodium retention during active childhood NS. Sodium 156-162 plasminogen Homo sapiens 76-83 33442688-2 2021 Plasmin, and other host proteases, may cleave the furin site of SARS-CoV-2 S protein and gamma subunits of epithelial sodium channels (gamma ENaC), resulting in an increment in virus infectivity and channel activity. Sodium 118-124 plasminogen Homo sapiens 0-7 23344662-4 2013 Recent clinical and experimental data indicate that proteinuria may mediate sodium retention and hypertension via plasmin-mediated activation of the epithelial sodium channel. Sodium 76-82 plasminogen Homo sapiens 114-121 21670672-8 2011 SUMMARY: The discovery of serine protease-mediated activation of renal ENaC in physiological and pathophysiological conditions opens the way for new understanding of the pathogenesis of proteinuric sodium retention, which may involve plasmin and present several potential new drug targets. Sodium 198-204 plasminogen Homo sapiens 234-241 21466573-0 2012 Proteinuric diseases with sodium retention: Is plasmin the link? Sodium 26-32 plasminogen Homo sapiens 47-54 31269481-10 2019 CONCLUSIONS: Our study identifies uPLG-PL abundance as an independent influencing factor of edema in adult NS patients, and supports the conclusion that plasmin-dependent ENaC activation is an important pathophysiological mechanism of sodium retention and edema formation in humans with NS. Sodium 235-241 plasminogen Homo sapiens 153-160 32232733-3 2020 Understanding of the pathophysiology of edema is still evolving with recent research elucidating newer mechanism of sodium retention through plasmin mediated epithelial sodium channel activation in collecting duct. Sodium 116-122 plasminogen Homo sapiens 141-148 31230006-4 2019 Plasmin may activate the epithelial sodium channel and cause impaired sodium excretion and contribute to hypertension. Sodium 36-42 plasminogen Homo sapiens 0-7 31269481-0 2019 Association of Urinary Plasminogen-Plasmin with Edema and Epithelial Sodium Channel Activation in Patients with Nephrotic Syndrome. Sodium 69-75 plasminogen Homo sapiens 23-30 31269481-1 2019 BACKGROUND: Previous animal experiments and small human studies suggest that urinary plasmin can activate the epithelial sodium channel (ENaC) and contribute to sodium retention in nephrotic syndrome (NS), but this however is not well studied in clinical settings, and its relevance to edema formation is not well characterized in humans. Sodium 121-127 plasminogen Homo sapiens 85-92 31269481-1 2019 BACKGROUND: Previous animal experiments and small human studies suggest that urinary plasmin can activate the epithelial sodium channel (ENaC) and contribute to sodium retention in nephrotic syndrome (NS), but this however is not well studied in clinical settings, and its relevance to edema formation is not well characterized in humans. Sodium 161-167 plasminogen Homo sapiens 85-92 29305116-3 2018 Plasmin activates the epithelial sodium channel in the collecting ducts potentially causing impaired sodium excretion, suppression of the renin-angiotensin-aldosterone system, and hypertension in PE. Sodium 33-39 plasminogen Homo sapiens 0-7