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ST2 cardiac biomarker

Gromeromd — Sat, 14 Nov 2026 21:40:14 GMT

The ST2/IL-33 Axis in Immune Cells in Inflammatory Diseases

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	ST2 is a member of the interleukin 1 receptor family. The ST2 protein has two isoforms and is directly implicated in the progression of cardiac disease: a soluble form (referred to as soluble ST2 or sST2) and a membrane-bound receptor form (referred to as the ST2 receptor or ST2L). When the myocardium is stretched, the ST2 gene is upregulated, increasing the concentration of circulating soluble ST2.<ref name="doi=10.1016/j.jchf.2012.10.002"/> The ligand for ST2 is the cytokine Interleukin-33(IL-33). Binding of IL-33 to the ST2 receptor, in response to cardiac disease or injury, such as an ischemic event, elicits a cardioprotective effect resulting in preserved cardiac function. This cardioprotective IL-33 signal is counterbalanced by the level of soluble ST2, which binds IL-33 and makes it unavailable to the ST2 receptor for cardioprotective signaling. As a result, the heart is subjected to greater stress in the presence of high levels of soluble ST2.		ST2 is a member of the interleukin 1 receptor family. The ST2 protein has two isoforms and is directly implicated in the progression of cardiac disease: a soluble form (referred to as soluble ST2 or sST2) and a membrane-bound receptor form (referred to as the ST2 receptor or ST2L). When the myocardium is stretched, the ST2 gene is upregulated, increasing the concentration of circulating soluble ST2.<ref name="doi=10.1016/j.jchf.2012.10.002"/> The ligand for ST2 is the cytokine Interleukin-33(IL-33). Binding of IL-33 to the ST2 receptor, in response to cardiac disease or injury, such as an ischemic event, elicits a cardioprotective effect resulting in preserved cardiac function. This cardioprotective IL-33 signal is counterbalanced by the level of soluble ST2, which binds IL-33 and makes it unavailable to the ST2 receptor for cardioprotective signaling. As a result, the heart is subjected to greater stress in the presence of high levels of soluble ST2.

	== Correlation with ~~mortality~~ ==		== Correlation with Mortality ==

	Published and peer-reviewed findings indicate that ST2 is a predictor of [[death\|mortality]] at presentation.<ref name="pmid18480207">{{cite journal \| author = Braunwald E \| title = Biomarkers in heart failure \| journal = N. Engl. J. Med. \| volume = 358 \| issue = 20 \| pages = 2148–59 \|date=May 2008 \| pmid = 18480207 \| doi = 10.1056/NEJMra0800239 }}</ref> Studies have shown patients with ST2 levels above a clinical threshold consistently have a much higher risk of mortality while, equally important, patients with ST2 levels below threshold have a very low risk of mortality.<ref name="pmid21178018">{{cite journal \|vauthors=Ky B, French B, McCloskey K, Rame JE, McIntosh E, Shahi P, Dries DL, Tang WH, Wu AH, Fang JC, Boxer R, Sweitzer NK, Levy WC, Goldberg LR, Jessup M, Cappola TP \| title = High-sensitivity ST2 for prediction of adverse outcomes in chronic heart failure \| journal = Circ Heart Fail \| volume = 4 \| issue = 2 \| pages = 180–7 \|date=March 2011 \| pmid = 21178018 \| pmc = 3163169 \| doi = 10.1161/CIRCHEARTFAILURE.110.958223 }}</ref><ref name="pmid22096031">{{cite journal \|vauthors=Kohli P, Bonaca MP, Kakkar R, Kudinova AY, Scirica BM, Sabatine MS, Murphy SA, Braunwald E, Lee RT, Morrow DA \| title = Role of ST2 in Non-ST-Elevation Acute Coronary Syndrome in the MERLIN-TIMI 36 Trial \| journal = Clin. Chem. \| volume = 58\| issue = 1\| pages = 257–66\|date=November 2011 \| pmid = 22096031 \| doi = 10.1373/clinchem.2011.173369 \| pmc = 4277435}}</ref> Although it has been shown that ST2 concentrations correlate with heart failure severity<ref name="pmid20804518">{{cite journal \|vauthors=Socrates T, deFilippi C, Reichlin T, Twerenbold R, Breidhardt T, Noveanu M, Potocki M, Reiter M, Arenja N, Heinisch C, Meissner J, Jaeger C, Christenson R, Mueller C \| title = Interleukin family member ST2 and mortality in acute dyspnoea \| journal = J. Intern. Med. \| volume = 268 \| issue = 5 \| pages = 493–500 \|date=November 2010 \| pmid = 20804518 \| doi = 10.1111/j.1365-2796.2010.02263.x }}</ref> there is no level that perfectly separates patients with and without heart failure for disease diagnosis. However, as a prognostic marker it has been clearly shown that patients are at a higher risk of adverse outcomes when ST2 levels are above a cutoff value of 35 ng/mL.<ref name="pmid21178018"/>		Published and peer-reviewed findings indicate that ST2 is a predictor of [[death\|mortality]] at presentation.<ref name="pmid18480207">{{cite journal \| author = Braunwald E \| title = Biomarkers in heart failure \| journal = N. Engl. J. Med. \| volume = 358 \| issue = 20 \| pages = 2148–59 \|date=May 2008 \| pmid = 18480207 \| doi = 10.1056/NEJMra0800239 }}</ref> Studies have shown patients with ST2 levels above a clinical threshold consistently have a much higher risk of mortality while, equally important, patients with ST2 levels below threshold have a very low risk of mortality.<ref name="pmid21178018">{{cite journal \|vauthors=Ky B, French B, McCloskey K, Rame JE, McIntosh E, Shahi P, Dries DL, Tang WH, Wu AH, Fang JC, Boxer R, Sweitzer NK, Levy WC, Goldberg LR, Jessup M, Cappola TP \| title = High-sensitivity ST2 for prediction of adverse outcomes in chronic heart failure \| journal = Circ Heart Fail \| volume = 4 \| issue = 2 \| pages = 180–7 \|date=March 2011 \| pmid = 21178018 \| pmc = 3163169 \| doi = 10.1161/CIRCHEARTFAILURE.110.958223 }}</ref><ref name="pmid22096031">{{cite journal \|vauthors=Kohli P, Bonaca MP, Kakkar R, Kudinova AY, Scirica BM, Sabatine MS, Murphy SA, Braunwald E, Lee RT, Morrow DA \| title = Role of ST2 in Non-ST-Elevation Acute Coronary Syndrome in the MERLIN-TIMI 36 Trial \| journal = Clin. Chem. \| volume = 58\| issue = 1\| pages = 257–66\|date=November 2011 \| pmid = 22096031 \| doi = 10.1373/clinchem.2011.173369 \| pmc = 4277435}}</ref> Although it has been shown that ST2 concentrations correlate with heart failure severity<ref name="pmid20804518">{{cite journal \|vauthors=Socrates T, deFilippi C, Reichlin T, Twerenbold R, Breidhardt T, Noveanu M, Potocki M, Reiter M, Arenja N, Heinisch C, Meissner J, Jaeger C, Christenson R, Mueller C \| title = Interleukin family member ST2 and mortality in acute dyspnoea \| journal = J. Intern. Med. \| volume = 268 \| issue = 5 \| pages = 493–500 \|date=November 2010 \| pmid = 20804518 \| doi = 10.1111/j.1365-2796.2010.02263.x }}</ref> there is no level that perfectly separates patients with and without heart failure for disease diagnosis. However, as a prognostic marker it has been clearly shown that patients are at a higher risk of adverse outcomes when ST2 levels are above a cutoff value of 35 ng/mL.<ref name="pmid21178018"/>
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	ST2 is an active participant in the cardiac [[Ventricular remodeling\|remodeling]] pathway and could identify which patients will respond to [[Eplerenone]], or other therapies that reverse myocardial [[fibrosis]].<ref name="pmid20117403">{{cite journal \|vauthors=Weir RA, Miller AM, Murphy GE, Clements S, Steedman T, Connell JM, McInnes IB, Dargie HJ, McMurray JJ \| title = Serum soluble ST2: a potential novel mediator in left ventricular and infarct remodeling after acute myocardial infarction \| journal = J Am Coll Cardiol \| volume = 55 \| issue = 3 \| pages = 243–50 \|date=January 2010 \| pmid = 20117403 \| doi = 10.1016/j.jacc.2009.08.047}}</ref>		ST2 is an active participant in the cardiac [[Ventricular remodeling\|remodeling]] pathway and could identify which patients will respond to [[Eplerenone]], or other therapies that reverse myocardial [[fibrosis]].<ref name="pmid20117403">{{cite journal \|vauthors=Weir RA, Miller AM, Murphy GE, Clements S, Steedman T, Connell JM, McInnes IB, Dargie HJ, McMurray JJ \| title = Serum soluble ST2: a potential novel mediator in left ventricular and infarct remodeling after acute myocardial infarction \| journal = J Am Coll Cardiol \| volume = 55 \| issue = 3 \| pages = 243–50 \|date=January 2010 \| pmid = 20117403 \| doi = 10.1016/j.jacc.2009.08.047}}</ref>

	== Clinical ~~utility~~ ==		== Clinical Utility ==

	* ST2 has considerable prognostic value and is used as an aid for risk [[stratified medicine\|stratification]] in identifying patients who are at high risk of mortality and [http://en.wiktionary.org/wiki/rehospitalization rehospitalization] in patients diagnosed with heart failure.<ref name="pmid20875357">{{cite journal \|vauthors=Bayes-Genis A, Pascual-Figal D, Januzzi JL, Maisel A, Casas T, Valdés Chávarri M, Ordóñez-Llanos J \| title = Soluble ST2 monitoring provides additional risk stratification for outpatients with decompensated heart failure \| journal = Rev Esp Cardiol \| volume = 63 \| issue = 10 \| pages = 1171–8 \|date=October 2010 \| pmid = 20875357 \| doi = 10.1016/s1885-5857(10)70231-0}}</ref>		* ST2 has considerable prognostic value and is used as an aid for risk [[stratified medicine\|stratification]] in identifying patients who are at high risk of mortality and [http://en.wiktionary.org/wiki/rehospitalization rehospitalization] in patients diagnosed with heart failure.<ref name="pmid20875357">{{cite journal \|vauthors=Bayes-Genis A, Pascual-Figal D, Januzzi JL, Maisel A, Casas T, Valdés Chávarri M, Ordóñez-Llanos J \| title = Soluble ST2 monitoring provides additional risk stratification for outpatients with decompensated heart failure \| journal = Rev Esp Cardiol \| volume = 63 \| issue = 10 \| pages = 1171–8 \|date=October 2010 \| pmid = 20875357 \| doi = 10.1016/s1885-5857(10)70231-0}}</ref>
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	* Repeated measurements of ST2 may aid in clinical decision-making.<ref name="pmid20875357"/><ref name="pmid18995177">{{cite journal \|vauthors=Boisot S, Beede J, Isakson S, Chiu A, Clopton P, Januzzi J, Maisel AS, Fitzgerald RL \| title = Serial sampling of ST2 predicts 90-day mortality following destabilized heart failure \| journal = J. Card. Fail. \| volume = 14 \| issue = 9 \| pages = 732–8 \|date=November 2008 \| pmid = 18995177 \| doi = 10.1016/j.cardfail.2008.06.415 }}</ref>		* Repeated measurements of ST2 may aid in clinical decision-making.<ref name="pmid20875357"/><ref name="pmid18995177">{{cite journal \|vauthors=Boisot S, Beede J, Isakson S, Chiu A, Clopton P, Januzzi J, Maisel AS, Fitzgerald RL \| title = Serial sampling of ST2 predicts 90-day mortality following destabilized heart failure \| journal = J. Card. Fail. \| volume = 14 \| issue = 9 \| pages = 732–8 \|date=November 2008 \| pmid = 18995177 \| doi = 10.1016/j.cardfail.2008.06.415 }}</ref>

	== The ST2 ~~test~~ ==		== The ST2 Test ==
	ST2 is measured by an [[immunoassay]], commercially marketed as the Presage ST2 Assay by Critical Diagnostics of San Diego, California.<ref name="urlCritical Diagnostics">{{cite web \| url = http://www.criticaldiagnostics.com/news-FDA-Approval-2011.html \| title = Critical Diagnostics \| date = \| work = \| publisher = Critical Diagnostics \| accessdate = }}</ref> The assay has [[Food and Drug Administration]] approval and a [[CE Mark]].<ref name="url510(k) Premarket Notification">{{cite web \| url = http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMN/pmn.cfm?ID=36927 \| title = 510(k) Premarket Notification \| date = \| work = \| publisher = United States Food and Drug Administration \| accessdate = }}</ref>		ST2 is measured by an [[immunoassay]], commercially marketed as the Presage ST2 Assay by Critical Diagnostics of San Diego, California.<ref name="urlCritical Diagnostics">{{cite web \| url = http://www.criticaldiagnostics.com/news-FDA-Approval-2011.html \| title = Critical Diagnostics \| date = \| work = \| publisher = Critical Diagnostics \| accessdate = }}</ref>

			The assay has [[Food and Drug Administration]] approval and a [[CE Mark]].<ref name="url510(k) Premarket Notification">{{cite web \| url = http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMN/pmn.cfm?ID=36927 \| title = 510(k) Premarket Notification \| date = \| work = \| publisher = United States Food and Drug Administration \| accessdate = }}</ref>

			== '''The ST2/IL-33 Axis in Immune Cells''' '''in Inflammatory Disease''' ==
			* '''Il1rl1 (also known as ST2)''' is a member of the IL-1 superfamily, and its ligand IL-33. ST2 exists in two forms as splice variants: a soluble form (sST2), which acts as a decoy receptor, sequesters free IL-33, and does not signal, and a membrane-bound form (ST2), that activates the MyD88/NF-κB signaling pathway to enhance mast cell, Th2, regulatory T cell (Treg), and innate lymphoid cell type 2 functions.<ref>''Griesenauer B and Paczesny S (2017) The ST2/IL-33 Axis in Immune Cells during Inflammatory Diseases. Front. Immunol. 8:475. doi: 10.3389/fimmu.2017.00475''</ref>
			* '''sST2 levels''' are increased in patients with inflammatory bowel disease, acute cardiac and small bowel transplant allograft rejection, colon and gastric cancers, gut mucosal damage during viral infection, pulmonary disease, heart disease, and graft-versus-host disease.
			* Recently, sST2 has been shown to be secreted by '''intestinal pro-inflammatory T cells''' during gut inflammation. <ref>''Griesenauer B and Paczesny S (2017) The ST2/IL-33 Axis in Immune Cells during Inflammatory Diseases. Front. Immunol. 8:475. doi: 10.3389/fimmu.2017.00475''</ref>

	==References==		==References==

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Anum Ijaz — Thu, 12 Nov 2026 15:09:00 GMT

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	'''Recommended indications (R2):'''		'''Recommended indications (R2):'''
	* Somatotrophinoma or prolactinoma diagnosed at or before 18 years of age.		* Somatotrophinoma or [[prolactinoma]] diagnosed at or before 18 years of age.
	* A personal history of pituitary adenoma and a blood relative with a pituitary adenoma.		* A personal history of pituitary adenoma and a blood relative with a pituitary adenoma.
	* A personal or family history of non-pituitary tumors associated with an established pituitary tumor predisposition gene.		* A personal or family history of non-pituitary tumors associated with an established pituitary tumor predisposition gene.

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User:Dr Muhammad Saad

Dr Muhammad Saad — Wed, 11 Nov 2026 08:34:44 GMT

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	==Current Position==		==Current Position==
	* Scholar/Editor ~~and Mentor~~ at '''WikiDoc.org'''		* Scholar/Editor at '''WikiDoc.org'''
	I create original content on my areas of interest and refresh older chapters to keep the medical information current.		I create original content on my areas of interest and refresh older chapters to keep the medical information current.

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	==Clinical Experience==		==Clinical Experience==

	* '''Liaquat University of Medical & Health Sciences, Jamshoro, Pakistan (01/~~2026~~ - Current)'''		* '''Liaquat University of Medical & Health Sciences, Jamshoro, Pakistan (03/2025 - Current)'''

	'''Position:''' Resident Physician		'''Position:''' Resident Physician
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	'''Supervisor Attending:''' Dr. Moona Humaira, MBBS, FCPS		'''Supervisor Attending:''' Dr. Moona Humaira, MBBS, FCPS

	* '''~~inova loudoun hospital~~ (07/2026 - 07/~~2022~~)'''		* '''Abington Memorial Hospital, PA (08/2026 - 08/2026)'''

	'''Position:''' Medical Observer		'''Position:''' Medical Observer

	'''Supervisor Attending:''' Dr. ~~Rauf Chaudhry~~, MD.		'''Supervisor Attending:''' Dr. Sunil Nair, MD.

	*'''~~Brown University Health~~ (06/2026 - 06/~~2022~~)'''		*'''Baylor Scott and White Medical Centre, Grapevine, TX (07/2026 - 08/2026)'''

	'''Position:''' Medical Observer		'''Position:''' Medical Observer

	'''Supervisor Attending:''' Dr. ~~Farukhuddin~~ MD.		'''Supervisor Attending:''' Dr. Arshad A Quddoos MD.

	* '''~~Liaquat University Civil Hospital~~, ~~Hyderabad/Jamshoro Pakistan~~ (05/~~2023~~ - 12/~~2025~~)'''		* '''Norman Endocrinology Associates, Norman, OK(06/2026 - 07/2026)'''

	'''Position:''' Medical ~~Officer with Dept. of Neurology and General Medicine~~		'''Position:''' Medical Observer

	~~'''Supervisor Attending:''' Prof. Dr. Manzoor Ali Lakhair, MBBS, FCPS.; Dr. Muhammad Aslam Rind, MBBS, FCPS, FRCP.~~

	* '''Carondelet St. Joseph’s Hospital, Tucson, AZ (06/2025 - 06/2025)'''

	~~'''Position:'''~~ Observer

	~~'''Supervisor Attending:''' Dr. Fahad J. Laghari, MD.~~

	* '''~~Charleston Area Medical Center, Charleston, WV (05/2025 - 05/2025)~~'''		'''Supervisor Attending:''' Dr. Lubna Mirza, MD.

	'''~~Position:~~''' ~~Observer~~		* '''Hashim Medical City Hospital, Hyderabad, Pakistan(09/2024 - 02/2025)'''

	'''~~Supervisor Attending~~:''' ~~Dr. Suzanne Crandall, DO, AOA.~~		'''Position:''' Medical Officer in Gastroenterology department

	* '''~~Boston Medical Center-South, Brockton, MA (04/2025 - 04/2025)~~'''		'''Supervisor Attending:''' Dr. Ai Akbar Siddiqui, FCPS

	'''~~Position:~~''' ~~Observer~~		* '''Liaquat University Civil Hospital, Hyderabad/Jamshoro Pakistan (05/2023 - 05/2024)'''

	'''~~Supervisor Attending~~:''' ~~Dr. Terri Spenser, MD.~~		'''Position:''' House Officer

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Amna Riaz — Wed, 11 Nov 2026 02:48:31 GMT

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Cell-cycle box gene transcriptions

Marshallsumter — Tue, 10 Nov 2026 08:43:42 GMT

CCB variant samplings

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	==CCB variant samplings==		==CCB variant samplings==
	{{main\|Model samplings}}		{{main\|Model samplings}}
			[[Cell-cycle box gene transcriptions#CCB variant samplings\|CCB variant samplings]]

	Copying a responsive elements consensus sequence CACGAAA, ACGAAA and C-CGAAA and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs. Actual consensus sequences to conform should contain CACGAAA, ACGAAA or CCGAAA.		Copying a responsive elements consensus sequence CACGAAA, ACGAAA and C-CGAAA and putting the sequence in "⌘F" finds none between ZNF497 and A1BG or none between ZSCAN22 and A1BG as can be found by the computer programs. Actual consensus sequences to conform should contain CACGAAA, ACGAAA or CCGAAA.

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Back pain differential diagnosis

Elizabeth Nguyen — Sun, 08 Nov 2026 06:49:07 GMT

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Back pain causes

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Back pain epidemiology and demographics

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