Abstract
Introduction: Incisional hernias (IH) arise as a complication of patients undergoing laparotomy. Current literature has assessed the role of extracellular matrix (ECM) disorganization, alterations in type I and type III collagen, matrix metalloproteinases, and tissue inhibitors of metalloproteases on IH. However, there is limited information on the underlying molecular mechanisms that lead to ECM disorganization. Areas covered: We critically reviewed the literature surrounding IH and ECM disorganization and offer a novel pathway that may be the underlying mechanism resulting in ECM disorganization and the immunopathogenesis of IH. Expert opinion: High mobility group box-1 (HMGB-1), a damage-associated molecular pattern, plays an important role in the sterile inflammatory pathway and has been linked to ECM disorganization and the triggering of the NLRP3 inflammasome. Further research to investigate the role of HMGB-1 in the molecular pathogenesis of IH would be critical in identifying novel therapeutic targets in the management of IH formation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 791-800 |
| Number of pages | 10 |
| Journal | Expert Review of Clinical Immunology |
| Volume | 15 |
| Issue number | 7 |
| DOIs | |
| State | Published - Jul 3 2019 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Immunology
Cite this
Novel understanding of high mobility group box-1 in the immunopathogenesis of incisional hernias. / Larsen, Nicholas K.; Reilly, Matthew J.; Thankam, Finosh G.; Fitzgibbons, Robert Joseph; Agrawal, Devendra K.
In: Expert Review of Clinical Immunology, Vol. 15, No. 7, 03.07.2019, p. 791-800.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Novel understanding of high mobility group box-1 in the immunopathogenesis of incisional hernias
AU - Larsen, Nicholas K.
AU - Reilly, Matthew J.
AU - Thankam, Finosh G.
AU - Fitzgibbons, Robert Joseph
AU - Agrawal, Devendra K.
PY - 2019/7/3
Y1 - 2019/7/3
N2 - Introduction: Incisional hernias (IH) arise as a complication of patients undergoing laparotomy. Current literature has assessed the role of extracellular matrix (ECM) disorganization, alterations in type I and type III collagen, matrix metalloproteinases, and tissue inhibitors of metalloproteases on IH. However, there is limited information on the underlying molecular mechanisms that lead to ECM disorganization. Areas covered: We critically reviewed the literature surrounding IH and ECM disorganization and offer a novel pathway that may be the underlying mechanism resulting in ECM disorganization and the immunopathogenesis of IH. Expert opinion: High mobility group box-1 (HMGB-1), a damage-associated molecular pattern, plays an important role in the sterile inflammatory pathway and has been linked to ECM disorganization and the triggering of the NLRP3 inflammasome. Further research to investigate the role of HMGB-1 in the molecular pathogenesis of IH would be critical in identifying novel therapeutic targets in the management of IH formation.
AB - Introduction: Incisional hernias (IH) arise as a complication of patients undergoing laparotomy. Current literature has assessed the role of extracellular matrix (ECM) disorganization, alterations in type I and type III collagen, matrix metalloproteinases, and tissue inhibitors of metalloproteases on IH. However, there is limited information on the underlying molecular mechanisms that lead to ECM disorganization. Areas covered: We critically reviewed the literature surrounding IH and ECM disorganization and offer a novel pathway that may be the underlying mechanism resulting in ECM disorganization and the immunopathogenesis of IH. Expert opinion: High mobility group box-1 (HMGB-1), a damage-associated molecular pattern, plays an important role in the sterile inflammatory pathway and has been linked to ECM disorganization and the triggering of the NLRP3 inflammasome. Further research to investigate the role of HMGB-1 in the molecular pathogenesis of IH would be critical in identifying novel therapeutic targets in the management of IH formation.
UR - http://www.scopus.com/inward/record.url?scp=85067618449&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85067618449&partnerID=8YFLogxK
U2 - 10.1080/1744666X.2019.1608822
DO - 10.1080/1744666X.2019.1608822
M3 - Review article
VL - 15
SP - 791
EP - 800
JO - Expert Review of Clinical Immunology
JF - Expert Review of Clinical Immunology
SN - 1744-666X
IS - 7
ER -