Editing Plasmin (section)

== Pathology ==

Plasmin deficiency may lead to [[thrombosis]], as the clots are not adequately degraded. Plasminogen deficiency in mice leads to defective liver repair,<ref>{{cite journal | vauthors = Bezerra JA, Bugge TH, Melin-Aldana H, Sabla G, Kombrinck KW, Witte DP, Degen JL | title = Plasminogen deficiency leads to impaired remodeling after a toxic injury to the liver | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 96 | issue = 26 | pages = 15143–15148 | date = December 1999 | pmid = 10611352 | pmc = 24787 | doi = 10.1073/pnas.96.26.15143 | doi-access = free | bibcode = 1999PNAS...9615143B }}</ref> defective wound healing, reproductive abnormalities.<ref>{{cite journal | vauthors = Romer J, Bugge TH, Pyke C, Lund LR, Flick MJ, Degen JL, Dano K | title = Impaired wound healing in mice with a disrupted plasminogen gene | journal = Nature Medicine | volume = 2 | issue = 3 | pages = 287–292 | date = March 1996 | pmid = 8612226 | doi = 10.1038/nm0396-287 | s2cid = 29981847 }}
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<ref>{{cite journal | vauthors = Ploplis VA, Carmeliet P, Vazirzadeh S, Van Vlaenderen I, Moons L, Plow EF, Collen D | title = Effects of disruption of the plasminogen gene on thrombosis, growth, and health in mice | journal = Circulation | volume = 92 | issue = 9 | pages = 2585–2593 | date = November 1995 | pmid = 7586361 | doi = 10.1161/01.cir.92.9.2585 | doi-access =  }}
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In humans, a rare disorder called [[plasminogen deficiency type I]] ({{OMIM|217090}}) is caused by mutations of the ''PLG'' gene and is often manifested by [[ligneous conjunctivitis]].<ref>{{cite journal | vauthors = Schuster V, Hügle B, Tefs K | title = Plasminogen deficiency | journal = Journal of Thrombosis and Haemostasis | volume = 5 | issue = 12 | pages = 2315–2322 | date = December 2007 | pmid = 17900274 | doi = 10.1111/j.1538-7836.2007.02776.x | doi-access = free }}</ref>

A rare [[missense mutation]] within the kringle 3 domain of plasminogen, resulting in a novel type of dysplasminogenemia, represents the molecular basis of a subtype of hereditary angioedema with normal C1-inhibitor;<ref name="Dewald">{{cite journal | vauthors = Dewald G | title = A missense mutation in the plasminogen gene, within the plasminogen kringle 3 domain, in hereditary angioedema with normal C1 inhibitor | journal = Biochemical and Biophysical Research Communications | volume = 498 | issue = 1 | pages = 193–198 | date = March 2018 | pmid = 29548426 | doi = 10.1016/j.bbrc.2017.12.060 }}
</ref> the mutation creates a new lysine-binding site within kringle 3 and alters the glycosylation of plasminogen.<ref name="Dewald" /> The mutant plasminogen protein has been shown to be a highly efficient kininogenase that directly releases bradykinin from high- and low-molecular-weight kininogen.<ref>{{cite journal | vauthors = Dickeson SK, Kumar S, Sun MF, Mohammed BM, Phillips DR, Whisstock JC, Quek AJ, Feener EP, Law RH, Gailani D | display-authors = 6 | title = A mechanism for hereditary angioedema caused by a lysine 311-to-glutamic acid substitution in plasminogen | journal = Blood | volume = 139 | issue = 18 | pages = 2816–2829 | date = May 2022 | pmid = 35100351 | doi = 10.1182/blood.2021012945 | pmc = 9074402 | doi-access = free }}
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