The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Antioxidant mechanism of heme oxygenase-1 involves an increase in superoxide dismutase and catalase in experimental diabetes
Abstract
Increased heme oxygenase (HO)-1 activity attenuates endothelial cell apoptosis and decreases superoxide anion (O 2−) formation in experimental diabetes by unknown mechanisms. We examined the effect of HO-1 protein and HO activity on extracellular SOD (EC-SOD), catalase, O 2−, inducible nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) levels and vascular responses to ACh in control and diabetic rats. Vascular EC-SOD and plasma catalase activities were significantly reduced in diabetic compared with nondiabetic rats ( P < 0.05). Upregulation of HO-1 expression by intermittent administration of cobalt protoporphyrin, an inducer of HO-1 protein and activity, resulted in a robust increase in EC-SOD but no significant change in Cu-Zn-SOD. Administration of tin mesoporphyrin, an inhibitor of HO-1 activity, decreased EC-SOD protein. Increased HO-1 activity in diabetic rats was associated with a decrease in iNOS but increases in eNOS and plasma catalase activity. On the other hand, aortic ring segments from diabetic rats exhibited a significant reduction in vascular relaxation to ACh, which was reversed with cobalt protoporphyrin treatment. These data demonstrate that an increase in HO-1 protein and activity, i.e., CO and bilirubin production, in diabetic rats brings about a robust increase in EC-SOD, catalase, and eNOS with a concomitant increase in endothelial relaxation and a decrease in O 2−. These observations in experimental diabetes suggest that the vascular cytoprotective mechanism of HO-1 against oxidative stress requires an increase in EC-SOD and catalase.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“HO-1 improves endothelial dysfunction in diabetes (314) and has angiogenic properties (88).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [314]
Citations
Cites
Role of Oxidative Stress in Development of Complications in Diabetes
Baynes, J. (1991) · Diabetes · doi:10.2337/diab.40.4.405 · Cited by 3,791
Rajagopalan, S., Kurz, S. D., Münzel, T. F., Tarpey, M. M., Freeman, B. Α., Griendling, K. K., & Harrison, D. G. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118623 · Cited by 2,467
Vasa‐Nicotera, M., Fichtlscherer, S., Aicher, A., Adler, K., Urbich, C., Martin, H., Zeiher, A. M., & Dimmeler, S. (2001) · Circulation Research · doi:10.1161/hh1301.093953 · Cited by 2,328
Ferritin: a cytoprotective antioxidant strategem of endothelium.
Balla, G., Jacob, H., Balla, J., Rosenberg, M. E., Nath, K. A., Apple, F., Eaton, J. W., & Vercellotti, G. M. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)37165-0 · Cited by 1,097
Smooth muscle cell-derived carbon monoxide is a regulator of vascular cGMP.
Morita, T., Perrella, M. A., Lee, M. E., & Kourembanas, S. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.5.1475 · Cited by 712
Vascular protection: superoxide dismutase isoforms in the vessel wall.
Faraci, F., & Didion, S. (2004) · Arteriosclerosis, Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000133604.20182.cf · Cited by 528
Otterbein, L. E., Zuckerbraun, B. S., Haga, M., Liu, F., Song, R., Usheva, A., Stachulak, C., Bodyak, N. D., Smith, R. N., Csizmadia, E., et al. (2003) · Nature Medicine · doi:10.1038/nm817 · Cited by 527
Oxidation of Tetrahydrobiopterin by Peroxynitrite: Implications for Vascular Endothelial Function
Milstien, S., & Katušić, Z. S. (1999) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1999.1422 · Cited by 492
Otterbein, L. E., Kolls, J. K., Mantell, L. L., Cook, J. L., Alam, J., & Choi, A. M. K. (1999) · Journal of Clinical Investigation · doi:10.1172/jci5342 · Cited by 492
Brüne, B., & Ullrich, V. (1987) · Molecular Pharmacology · doi:10.1016/s0026-895x(25)13029-0 · Cited by 472
Cited by
Sorted by citations
Heme Oxygenase-1/Carbon Monoxide: From Basic Science to Therapeutic Applications
Ryter, S. W., Alam, J., & Choi, A. M. K. (2006) · Physiological Reviews · doi:10.1152/physrev.00011.2005 · Cited by 2,346
Mechanisms of Cell Death in Oxidative Stress
Ryter, S. W., Kim, H. P., Hoetzel, A., Park, J. W., Nakahira, K., Wang, X., & Choi, A. M. K. (2006) · Antioxidants and Redox Signaling · doi:10.1089/ars.2007.9.49 · Cited by 1,286
Pharmacological and Clinical Aspects of Heme Oxygenase
Abraham, N. G., & Kappas, A. (2008) · Pharmacological Reviews · doi:10.1124/pr.107.07104 · Cited by 1,115
Self-citationGonzález, P., Lozano, P., Ros, G., & Solano, F. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24119352 · Cited by 948
Sivitz, W. I., & Yorek, M. A. (2010) · Antioxidants & Redox Signaling · doi:10.1089/ars.2009.2531 · Cited by 742
Metadata
- Authors
- Turkseven, S., Kruger, A., Mingone, C. J., Kaminski, P., Inaba, M., Rodella, L. F., Ikehara, S., Wolin, M. S., & Abraham, N. G.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2005-08
- Volume
- 289
- Issue
- 2
- Pages
- H701-H707
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2160708843
- Cited by
- 256
- References
- 57
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 5 · 2023: 6 · 2022: 13 · 2021: 18 · 2020: 12 · 2019: 15 · 2018: 8 · 2017: 8 · 2016: 11 · 2015: 7 · 2014: 8 · 2013: 10 · 2012: 17
- FWCI
- 7.40
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System (Università degli Studi di Brescia) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL034300, HL 34300, HL55601)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heme Oxygenase-1 and Carbon Monoxide
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Hemoglobin structure and function
- Keywords
- heme oxygenase-1, superoxide dismutase, catalase, experimental diabetes, oxidative stress, endothelial nitric oxide synthase, inducible nitric oxide synthase, cobalt protoporphyrin, tin mesoporphyrin, endothelium-dependent relaxation, acetylcholine, vascular function, bilirubin, carbon monoxide, endothelial cell apoptosis
- MeSH terms
- Acetylcholine, Animals, Antioxidants, Aorta, Blood Vessels, Catalase, Cobalt, Diabetes Mellitus, Experimental, Endothelium, Vascular, Enzyme Induction, Heme Oxygenase (Decyclizing), Immunohistochemistry, Protoporphyrins, Superoxides, Superoxide Dismutase, Vasodilator Agents, Rats, Sprague-Dawley, Nitric Oxide Synthase, Rats, Heme Oxygenase-1, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
