Abstract
PURPOSE OF REVIEW: Heme oxygenase activity, possessed by an inducible heme oxygenase-1 (HO-1) and a constitutive isoform (HO-2), catalyzes the conversion of heme to biliverdin, liberates iron, and generates carbon monoxide. First shown in acute kidney injury (AKI), HO-1 is now recognized as a protectant against diverse insults in assorted tissues. This review summarizes recent contributions to the field of HO-1 and AKI. RECENT FINDINGS: Recent findings elucidate the following: the transcriptional regulation and significance of human HO-1 in AKI; the protective effects of HO-1 in age-dependent and sepsis-related AKI, cardiorenal syndromes, and acute vascular rejection in renal xenografts; the role of heme oxygenase in tubuloglomerular feedback and renal resistance to injury; the basis for cytoprotection by HO-1; the protective properties of ferritin and carbon monoxide; HO-1 and the AKI-chronic kidney disease transition; HO-1 as a biomarker in AKI; the role of HO-1 in mediating the protective effects of specific cytokines, stem cells, and therapeutic agents in AKI; and HO-2 as a protectant in AKI. SUMMARY: Recent contributions support, and elucidate the basis for, the induction of HO-1 as a protectant against AKI. Translating such therapeutic potential into a therapeutic reality requires well tolerated and effective modalities for upregulating HO-1 and/or administering its products, which, optimally, should be salutary even when AKI is already established.
Original language | English (US) |
---|---|
Pages (from-to) | 17-24 |
Number of pages | 8 |
Journal | Current Opinion in Nephrology and Hypertension |
Volume | 23 |
Issue number | 1 |
DOIs | |
State | Published - Jan 2014 |
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Keywords
- acute kidney injury
- acute renal failure
- cytoprotection
- heme oxygenase-1
ASJC Scopus subject areas
- Nephrology
- Internal Medicine
Cite this
Heme oxygenase-1 and acute kidney injury. / Nath, Karl A.
In: Current Opinion in Nephrology and Hypertension, Vol. 23, No. 1, 01.2014, p. 17-24.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Heme oxygenase-1 and acute kidney injury
AU - Nath, Karl A
PY - 2014/1
Y1 - 2014/1
N2 - PURPOSE OF REVIEW: Heme oxygenase activity, possessed by an inducible heme oxygenase-1 (HO-1) and a constitutive isoform (HO-2), catalyzes the conversion of heme to biliverdin, liberates iron, and generates carbon monoxide. First shown in acute kidney injury (AKI), HO-1 is now recognized as a protectant against diverse insults in assorted tissues. This review summarizes recent contributions to the field of HO-1 and AKI. RECENT FINDINGS: Recent findings elucidate the following: the transcriptional regulation and significance of human HO-1 in AKI; the protective effects of HO-1 in age-dependent and sepsis-related AKI, cardiorenal syndromes, and acute vascular rejection in renal xenografts; the role of heme oxygenase in tubuloglomerular feedback and renal resistance to injury; the basis for cytoprotection by HO-1; the protective properties of ferritin and carbon monoxide; HO-1 and the AKI-chronic kidney disease transition; HO-1 as a biomarker in AKI; the role of HO-1 in mediating the protective effects of specific cytokines, stem cells, and therapeutic agents in AKI; and HO-2 as a protectant in AKI. SUMMARY: Recent contributions support, and elucidate the basis for, the induction of HO-1 as a protectant against AKI. Translating such therapeutic potential into a therapeutic reality requires well tolerated and effective modalities for upregulating HO-1 and/or administering its products, which, optimally, should be salutary even when AKI is already established.
AB - PURPOSE OF REVIEW: Heme oxygenase activity, possessed by an inducible heme oxygenase-1 (HO-1) and a constitutive isoform (HO-2), catalyzes the conversion of heme to biliverdin, liberates iron, and generates carbon monoxide. First shown in acute kidney injury (AKI), HO-1 is now recognized as a protectant against diverse insults in assorted tissues. This review summarizes recent contributions to the field of HO-1 and AKI. RECENT FINDINGS: Recent findings elucidate the following: the transcriptional regulation and significance of human HO-1 in AKI; the protective effects of HO-1 in age-dependent and sepsis-related AKI, cardiorenal syndromes, and acute vascular rejection in renal xenografts; the role of heme oxygenase in tubuloglomerular feedback and renal resistance to injury; the basis for cytoprotection by HO-1; the protective properties of ferritin and carbon monoxide; HO-1 and the AKI-chronic kidney disease transition; HO-1 as a biomarker in AKI; the role of HO-1 in mediating the protective effects of specific cytokines, stem cells, and therapeutic agents in AKI; and HO-2 as a protectant in AKI. SUMMARY: Recent contributions support, and elucidate the basis for, the induction of HO-1 as a protectant against AKI. Translating such therapeutic potential into a therapeutic reality requires well tolerated and effective modalities for upregulating HO-1 and/or administering its products, which, optimally, should be salutary even when AKI is already established.
KW - acute kidney injury
KW - acute renal failure
KW - cytoprotection
KW - heme oxygenase-1
UR - http://www.scopus.com/inward/record.url?scp=84890560746&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84890560746&partnerID=8YFLogxK
U2 - 10.1097/01.mnh.0000437613.88158.d3
DO - 10.1097/01.mnh.0000437613.88158.d3
M3 - Article
C2 - 24275768
AN - SCOPUS:84890560746
VL - 23
SP - 17
EP - 24
JO - Current Opinion in Nephrology and Hypertension
JF - Current Opinion in Nephrology and Hypertension
SN - 1062-4821
IS - 1
ER -