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