Editing Myoglobin (section)

==Role in disease==
Myoglobin is released from damaged muscle tissue, which contain very high concentrations of myoglobin.<ref name="Berridge Van Vleet Herman 2013 pp. 1567–1665">{{cite book | vauthors = Berridge BR, Van Vleet JF, Herman E | title=Haschek and Rousseaux's Handbook of Toxicologic Pathology | chapter=Cardiac, Vascular, and Skeletal Muscle Systems | publisher=Elsevier | year=2013 | isbn=978-0-12-415759-0 | doi=10.1016/b978-0-12-415759-0.00046-7 | pages=1567–1665 | quote=Myoglobin is a low molecular weight oxygen binding heme protein that is found exclusively in heart and skeletal muscle cells.  In blood, myoglobin is bound primarily to plasma globulins, a complex which is filtered by the kidneys. If the plasma concentration exceeds the plasma binding capacity (1.5 mg/dl in humans), myoglobin begins to appear in the urine. High concentrations of myoglobin can change the color of the urine to a dark red-brown color.}}</ref> The released myoglobin enters the bloodstream, where high levels may indicate [[rhabdomyolysis]]. The myoglobin is filtered by the [[kidneys]], but is toxic to the renal tubular epithelium and so may cause [[acute kidney injury]].<ref name="renal">{{cite journal | vauthors = Naka T, Jones D, Baldwin I, Fealy N, Bates S, Goehl H, Morgera S, Neumayer HH, Bellomo R | title = Myoglobin clearance by super high-flux hemofiltration in a case of severe rhabdomyolysis: a case report | journal = Critical Care | volume = 9 | issue = 2 | pages = R90-5 | date = Apr 2005 | pmid = 15774055 | pmc = 1175920 | doi = 10.1186/cc3034 | doi-access = free }}</ref>  It is not the myoglobin itself that is toxic (it is a [[protoxin]]), but the ferrihemate portion that is dissociated from myoglobin in acidic environments (e.g., acidic urine, [[lysosome]]s).{{cn|date=June 2024}}

Myoglobin is a sensitive marker for muscle injury, making it a potential marker for [[myocardial infarction|heart attack]] in patients with [[chest pain]].<ref name="diagnosis">{{cite journal | vauthors = Weber M, Rau M, Madlener K, Elsaesser A, Bankovic D, Mitrovic V, Hamm C | title = Diagnostic utility of new immunoassays for the cardiac markers cTnI, myoglobin and CK-MB mass | journal = Clinical Biochemistry | volume = 38 | issue = 11 | pages = 1027–30 | date = Nov 2005 | pmid = 16125162 | doi = 10.1016/j.clinbiochem.2005.07.011 }}</ref> However, elevated myoglobin has low [[Sensitivity and specificity|specificity]] for [[myocardial infarction|acute myocardial infarction (AMI)]] and thus [[Creatine kinase|CK-MB]], [[Troponin|cardiac troponin]], [[Electrocardiogram|ECG]], and clinical signs should be taken into account to make the diagnosis.<ref name="Dasgupta Wahed 2014 pp. 127–144">{{cite book | vauthors = Dasgupta A, Wahed A | title=Clinical Chemistry, Immunology and Laboratory Quality Control | chapter=Cardiac Markers | publisher=Elsevier | year=2014 | isbn=978-0-12-407821-5 | doi=10.1016/b978-0-12-407821-5.00008-5 | pages=127–144 | quote=Myoglobin is a heme protein found in both skeletal and cardiac muscle. Myoglobin is typically released in the circulation as early as 1 h after myocardial infarction,... Myoglobin has poor clinical specificity due to the presence of large quantities of myoglobin in skeletal muscle. Some studies suggest adding the myoglobin test to the [[troponin I]] test in order to improve diagnostic value [4]. Myoglobin, being a small protein, is excreted in urine, and a high level of serum myoglobin is encountered in patients with acute renal failure ([[uremic syndrome]]). Acute renal failure is also a complication of rhabdomyolysis, ...}}</ref>