Mechanisms and therapeutic targets of ischemic acute kidney injury
Acute kidney injury (AKI) due to renal ischemia reperfusion (IR) is a major clinical problem without effective therapy and is a significant and frequent cause of morbidity and mortality during the perioperative period. Although the pathophysiology of ischemic AKI is not completely understood, severa...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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The Korean Society of Nephrology
2019-12-01
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| Series: | Kidney Research and Clinical Practice |
| Subjects: | |
| Online Access: | https://doi.org/10.23876/j.krcp.19.062 |
| _version_ | 1818188444409528320 |
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| author | Sang Jun Han H. Thomas Lee |
| author_facet | Sang Jun Han H. Thomas Lee |
| author_sort | Sang Jun Han |
| collection | DOAJ |
| description | Acute kidney injury (AKI) due to renal ischemia reperfusion (IR) is a major clinical problem without effective therapy and is a significant and frequent cause of morbidity and mortality during the perioperative period. Although the pathophysiology of ischemic AKI is not completely understood, several important mechanisms of renal IR-induced AKI have been studied. Renal ischemia and subsequent reperfusion injury initiates signaling cascades mediating renal cell necrosis, apoptosis, and inflammation, leading to AKI. Better understanding of the molecular and cellular pathophysiological mechanisms underlying ischemic AKI will provide more targeted approach to prevent and treat renal IR injury. In this review, we summarize important mechanisms of ischemic AKI, including renal cell death pathways and the contribution of endothelial cells, epithelial cells, and leukocytes to the inflammatory response during ischemic AKI. Additionally, we provide some updated potential therapeutic targets for the prevention or treatment of ischemic AKI, including Toll-like receptors, adenosine receptors, and peptidylarginine deiminase 4. Finally, we propose mechanisms of ischemic AKI-induced liver, intestine, and kidney dysfunction and systemic inflammation mainly mediated by Paneth cell degranulation as a potential explanation for the high mortality observed with AKI. |
| first_indexed | 2024-12-11T23:27:01Z |
| format | Article |
| id | doaj.art-8fbb50e6c84d4c54910aac9a099dbde0 |
| institution | Directory Open Access Journal |
| issn | 2211-9132 |
| language | English |
| last_indexed | 2024-12-11T23:27:01Z |
| publishDate | 2019-12-01 |
| publisher | The Korean Society of Nephrology |
| record_format | Article |
| series | Kidney Research and Clinical Practice |
| spelling | doaj.art-8fbb50e6c84d4c54910aac9a099dbde02022-12-22T00:46:09ZengThe Korean Society of NephrologyKidney Research and Clinical Practice2211-91322019-12-0138442744010.23876/j.krcp.19.062j.krcp.19.062Mechanisms and therapeutic targets of ischemic acute kidney injurySang Jun Han0H. Thomas Lee1Department of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USADepartment of Anesthesiology, College of Physicians and Surgeons of Columbia University, New York, NY, USAAcute kidney injury (AKI) due to renal ischemia reperfusion (IR) is a major clinical problem without effective therapy and is a significant and frequent cause of morbidity and mortality during the perioperative period. Although the pathophysiology of ischemic AKI is not completely understood, several important mechanisms of renal IR-induced AKI have been studied. Renal ischemia and subsequent reperfusion injury initiates signaling cascades mediating renal cell necrosis, apoptosis, and inflammation, leading to AKI. Better understanding of the molecular and cellular pathophysiological mechanisms underlying ischemic AKI will provide more targeted approach to prevent and treat renal IR injury. In this review, we summarize important mechanisms of ischemic AKI, including renal cell death pathways and the contribution of endothelial cells, epithelial cells, and leukocytes to the inflammatory response during ischemic AKI. Additionally, we provide some updated potential therapeutic targets for the prevention or treatment of ischemic AKI, including Toll-like receptors, adenosine receptors, and peptidylarginine deiminase 4. Finally, we propose mechanisms of ischemic AKI-induced liver, intestine, and kidney dysfunction and systemic inflammation mainly mediated by Paneth cell degranulation as a potential explanation for the high mortality observed with AKI.https://doi.org/10.23876/j.krcp.19.062acute kidney injuryapoptosisinflammationischemia reperfusion injurymechanismnecrosis |
| spellingShingle | Sang Jun Han H. Thomas Lee Mechanisms and therapeutic targets of ischemic acute kidney injury Kidney Research and Clinical Practice acute kidney injury apoptosis inflammation ischemia reperfusion injury mechanism necrosis |
| title | Mechanisms and therapeutic targets of ischemic acute kidney injury |
| title_full | Mechanisms and therapeutic targets of ischemic acute kidney injury |
| title_fullStr | Mechanisms and therapeutic targets of ischemic acute kidney injury |
| title_full_unstemmed | Mechanisms and therapeutic targets of ischemic acute kidney injury |
| title_short | Mechanisms and therapeutic targets of ischemic acute kidney injury |
| title_sort | mechanisms and therapeutic targets of ischemic acute kidney injury |
| topic | acute kidney injury apoptosis inflammation ischemia reperfusion injury mechanism necrosis |
| url | https://doi.org/10.23876/j.krcp.19.062 |
| work_keys_str_mv | AT sangjunhan mechanismsandtherapeutictargetsofischemicacutekidneyinjury AT hthomaslee mechanismsandtherapeutictargetsofischemicacutekidneyinjury |