Endothelial nitric oxide synthase overexpression attenuates myocardial reperfusion injury
Abstract
Previous studies indicate that deficiency of endothelial nitric oxide (NO) synthase (eNOS)-derived NO exacerbates myocardial reperfusion injury. We hypothesized that overexpression of eNOS would reduce the extent of myocardial ischemia-reperfusion (MI/R) injury. We investigated two distinct strains of transgenic (TG) mice overexpressing the eNOS gene (eNOS TG). Bovine eNOS was overexpressed in one strain (eNOS TG-Kobe), whereas the human eNOS gene was overexpressed in the other strain (eNOS TG-RT). Non-TG (NTG) and eNOS TG mice were subjected to 30 min of coronary artery occlusion followed by 24 h of reperfusion, and the extent of myocardial infarction was determined. Myocardial infarct size was reduced by 33% in the eNOS TG-Kobe strain (P < 0.05 vs. NTG) and by 32% in the eNOS TG-RT strain (P < 0.05 vs. NTG). However, postischemic cardiac function (cardiac output, fractional shortening) was not improved in the eNOS TG-Kobe mouse at 24 h of reperfusion [P = not significant (NS) vs. NTG]. In additional studies, eNOS TG-Kobe mice were subjected to 30 min of myocardial infarction and 7 days of reperfusion. Fractional shortening and the first derivative of left ventricular pressure were measured in eNOS TG-Kobe and NTG mice, and no significant differences in contractility were observed (P = NS) between the eNOS TG mice and NTG controls. Left ventricular end-diastolic pressure was significantly (P < 0.05 vs. NTG) reduced in the eNOS TG-Kobe strain at 7 days of reperfusion. The car…
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The protective effects of NO on cardiac ischemia/reperfusion injury depend on the local stock of nitrite and its subsequent reduction to NO at the critical moment when NOS activity is lacking under hypoxic conditions.
“Although the genetic overexpression of eNOS in mice attenuates myocardial infarction [98], in general, the protective effects of NO on cardiac ischemia/reperfusion injury depend on the local stock of nitrite and its subsequent reduction to NO at the critical moment when NOS activity is lacking under hypoxic conditions.”
From NO-Rich Diet for Lifestyle-Related Diseases (2015) · cites this paper as [98]
Cites
Furchgott, R. F., & Zawadzki, J. V. (1980) · Nature · doi:10.1038/288373a0 · Cited by 12,064 · see citing works
Nitric oxide: an endogenous modulator of leukocyte adhesion.
Kubes, P., Suzuki, M., & Granger, D. N. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.11.4651 · Cited by 3,052 · see citing works
Ignarro, L. J., Lippton, H., Edwards, J. C., Baricos, W. H., Hyman, A. L., Kadowitz, P. J., & Gruetter, C. A. (1981) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(25)32738-2 · Cited by 1,633 · cited 1× · see citing works
“NO promotes vasodilation (4, 8), regulates leukocyte-endothelial cell interactions (17), inhibits platelet adhesion and aggregation (9, 22), attenuates smooth muscle cell proliferation (7), and may modulate cardiac myocyte function (16).”
BackgroundNitric Oxide and Cardiac Function
Kelly, R. A., Balligand, J., & Smith, T. W. (1996) · Circulation Research · doi:10.1161/01.res.79.3.363 · Cited by 710 · see citing works
Mellion, B. T., Ignarro, L. J., Ohlstein, E. H., Pontecorvo, E., Hyman, A. L., & Kadowitz, P. (1981) · Blood · doi:10.1182/blood.v57.5.946.946 · Cited by 639 · see citing works
Janssens, S. P., Shimouchi, A., Quertermous, T., Bloch, D. B., & Bloch, K. D. (1992) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)42066-2 · Cited by 592 · see citing works
Nitric Oxide Donors and Cardiovascular Agents Modulating the Bioactivity of Nitric Oxide
Ignarro, L. J., Claudio Napoli, A., & Loscalzo, J. (2002) · Circulation Research · doi:10.1161/hh0102.102330 · Cited by 489 · see citing works
Modulation of ischemia/reperfusion-induced microvascular dysfunction by nitric oxide.
Kurose, I., Wolf, R., Grisham, M. B., & Granger, D. N. (1994) · Circulation Research · doi:10.1161/01.res.74.3.376 · Cited by 390 · see citing works
Ignarro, L. J., Buga, G. M., Liu, W., Bauer, P. M., Wu, G., & Soldato, P. D. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.071054698 · Cited by 331 · see citing works
The role of L-arginine in ameliorating reperfusion injury after myocardial ischemia in the cat.
Weyrich, A. S., Ma, X. L., & Lefer, A. M. (1992) · Circulation · doi:10.1161/01.cir.86.1.279 · Cited by 320 · see citing works
Ozaki, M., Kawashima, S., Yamashita, T., Hirase, T., Namiki, M., Inoue, N., Hirata, K., Yasui, H., Sakurai, H., Yoshida, Y., et al. (2002) · Journal of Clinical Investigation · doi:10.1172/jci15215 · Cited by 312 · see citing works
Self-citationOckaili, R. A., Salloum, F. N., Hawkins, J., & Kukreja, R. C. (2002) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00324.2002 · Cited by 292 · see citing works
Ohashi, Y., Kawashima, S., Hirata, K., Yamashita, T., Ishida, T., Inoue, N., Sakoda, T., Kurihara, H., Yazaki, Y., & Yokoyama, M. (1998) · Journal of Clinical Investigation · doi:10.1172/jci4394 · Cited by 278 · see citing works
Self-citationLefer, D. J., Nakanishi, K., Johnston, W. E., & Vinten‐Johansen, J. (1993) · Circulation · doi:10.1161/01.cir.88.5.2337 · Cited by 271 · see citing works
Self-citationOzaki, M., Kawashima, S., Yamashita, T., Hirase, T., Namiki, M., Inoue, N., Hirata, K.-I., Yasui, H., Sakurai, H., Yoshida, Y., et al. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0215215 · Cited by 268 · see citing works
Self-citationJones, S. P., Girod, W. G., Palazzo, A. J., Granger, D. N., Grisham, M. B., Jourd’heuil, D., Huang, P. L., & Lefer, D. J. (1999) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1999.276.5.h1567 · Cited by 265 · see citing works
Self-citationEndothelial nitric oxide synthase overexpression attenuates congestive heart failure in mice
Jones, S. P., Greer, J. J. M., van Haperen, R., Duncker, D. J., de Crom, R., & Lefer, D. J. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0837428100 · Cited by 229 · see citing works
Self-citationCardioprotective effects of authentic nitric oxide in myocardial ischemia with reperfusion
Johnson, G., Tsao, P. S., & Lefer, A. M. (1991) · Critical Care Medicine · doi:10.1097/00003246-199102000-00021 · Cited by 217 · see citing works
Intracoronary L-arginine during reperfusion improves endothelial function and reduces infarct size
Nakanishi, K., Vinten-Johansen, J., Lefer, D. J., Zhao, Z., Fowler, W. C., McGee, D. S., & Johnston, W. E. (1992) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1992.263.6.h1650 · Cited by 181 · see citing works
Self-citationZhao, T., Xi, L., Chelliah, J. C., Levasseur, J. E., & Kukreja, R. C. (2000) · Circulation · doi:10.1161/01.cir.102.8.902 · Cited by 152 · see citing works
Pabla, R., Buda, A. J., Flynn, D. M., Blessé, S. A., Shin, A. M., Curtis, M. J., & Lefer, D. J. (1996) · Circulation Research · doi:10.1161/01.res.78.1.65 · Cited by 142 · see citing works
Self-citationHeger, J., Gödecke, A., Flögel, U., Merx, M. W., Molojavyi, A., Kühn‐Velten, W. N., & Schrader, J. (2002) · Circulation Research · doi:10.1161/hh0102.102757 · Cited by 141 · see citing works
Biphasic response of cardiac NO synthase isoforms to ischemic preconditioning in conscious rabbits
Xuan, Y., Tang, X., Qiu, Y., Banerjee, S., Takano, H., Han, H. L., & Bolli, R. (2000) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.2000.279.5.h2360 · Cited by 140 · see citing works
Resistance to Endotoxin Shock in Transgenic Mice Overexpressing Endothelial Nitric Oxide Synthase
Yamashita, T., Kawashima, S., Ohashi, Y., Ozaki, M., Ueyama, T., Ishida, T., Inoue, N., Hirata, K., Akita, H., & Yokoyama, M. (2000) · Circulation · doi:10.1161/01.cir.101.8.931 · Cited by 140 · see citing works
Self-citationBrünner, F. (2002) · Cardiovascular Research · doi:10.1016/s0008-6363(02)00649-1 · Cited by 131 · see citing works
Brünner, F., Andrew, P., Wölkart, G., Zechner, R., & Mayer, B. (2001) · Circulation · doi:10.1161/hc5001.101966 · Cited by 122 · see citing works
Lorenz, J. N., & Robbins, J. M. (1997) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1997.272.3.h1137 · Cited by 109 · see citing works
van Haperen, R., de Waard, M., van Deel, E. D., Mees, B., Kutryk, M. B. J., van Aken, T., Hamming, J. F., Grosveld, F. G., Duncker, D. J., & de Crom, R. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m209477200 · Cited by 108 · see citing works
Kawashima, S., Yamashita, T., Ozaki, M., Ohashi, Y., Azumi, H., Inoue, N., Hirata, K., Hayashi, Y., Itoh, H., & Yokoyama, M. (2001) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.21.2.201 · Cited by 95 · see citing works
Self-citationYamashita, T., Kawashima, S., Ohashi, Y., Ozaki, M., Rikitake, Y., Inoue, N., Hirata, K., Akita, H., & Yokoyama, M. (2000) · Hypertension · doi:10.1161/01.hyp.36.1.97 · Cited by 93 · see citing works
Self-citationJones, S. P., Trocha, S. D., & Lefer, D. J. (2001) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/hq1201.099509 · Cited by 92 · see citing works
Self-citationInhibition of endothelium-derived relaxing factor enhances myocardial stunning in conscious dogs.
Hasebe, N., Shen, Y. T., & Vatner, S. F. (1993) · Circulation · doi:10.1161/01.cir.88.6.2862 · Cited by 80 · see citing works
Beneficial effects of SPM-5185, a cysteine-containing NO donor in myocardial ischemia-reperfusion
Siegfried, M. R., Carey, C. M., Ma, X. L., & Lefer, A. M. (1992) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1992.263.3.h771 · Cited by 75 · see citing works
Ozaki, M., Kawashima, S., Hirase, T., Yamashita, T., Namiki, M., Inoue, N., Hirata, K., & Yokoyama, M. (2002) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)62560-6 · Cited by 66 · see citing works
Self-citationLaumonnier, Y., Nadaud, S., Agrapart, M., & Soubrier, F. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.m004696200 · Cited by 62 · see citing works
Pabla, R., Buda, A. J., Flynn, D. M., Salzberg, D. B., & Lefer, D. J. (1995) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1995.269.3.h1113 · Cited by 51 · see citing works
Self-citationDraper, N. J., & Shah, A. M. (1997) · Journal of Molecular and Cellular Cardiology · doi:10.1006/jmcc.1996.0355 · Cited by 38 · see citing works
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Reactive oxygen species in cardiovascular disease
Sugamura, K., & Keaney (2011) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2011.05.004 · Cited by 769 · see citing works
“Consistent with eNOS as a protective factor, eNOS overexpression protects against MI and ischemic reperfusion injury compared to the wild-type phenotype [120, 121].”
BackgroundCytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver
Duranski, M. R., Greer, J. J. M., Dejam, A., Jaganmohan, S., Hogg, N., Langston, W., Patel, R. P., Yet, S.-F., Wang, X., Kevil, C. G., et al. (2005) · Journal of Clinical Investigation · doi:10.1172/jci22493 · Cited by 674 · see citing works
“More recently, we demonstrated that the severity of myocardial I/R injury is markedly exacerbated in mice completely deficient in eNOS ( eNOS –/– mice) (55), whereas mice with eNOS overexpression are protected against myocardial infarction and subsequent congestive heart failure (25, 26, 56).”
Self-citationShiva, S., Sack, M. N., Greer, J. J., Duranski, M., Ringwood, L. A., Burwell, L., Wang, X., MacArthur, P. H., Shoja, A., Raghavachari, N., et al. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070198 · Cited by 555 · see citing works
Self-citationThe ubiquitous role of nitric oxide in cardioprotection
Jones, S. P., & Bolli, R. (2006) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2005.09.011 · Cited by 434 · see citing works
Self-citationCalvert, J. W., Gundewar, S., Jha, S., Greer, J. J. M., Bestermann, W. H., Tian, R., & Lefer, D. J. (2008) · Diabetes · doi:10.2337/db07-1098 · Cited by 422 · see citing works
“Surgical ligation of the left coronary artery (LCA) was performed similar to methods described previously (23).”
Self-citationDietary nitrite supplementation protects against myocardial ischemia-reperfusion injury
Bryan, N. S., Calvert, J. W., Elrod, J. W., Gundewar, S., Ji, S. Y., & Lefer, D. J. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0706579104 · Cited by 347 · see citing works
Self-citationZordoky, B. N. M., Robertson, I. M., & Dyck, J. R. B. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2014.10.016 · Cited by 340 · see citing works
Novel Insights Into Hydrogen Sulfide–Mediated Cytoprotection
Calvert, J. W., Coetzee, W. A., & Lefer, D. J. (2009) · Antioxidants and Redox Signaling · doi:10.1089/ars.2009.2882 · Cited by 312 · see citing works
“Moreover, NO possesses a number of physiological properties that make it a potent cardioprotectivesignaling molecule (35).”
Self-citationCardioprotection by N -Acetylglucosamine Linkage to Cellular Proteins
Jones, S. P., Zachara, N. E., Ngoh, G. A., Hill, B. G., Teshima, Y., Bhatnagar, A., Hart, G. W., & Marbán, E. (2008) · Circulation · doi:10.1161/circulationaha.107.730515 · Cited by 258 · see citing works
Self-citationSphingosine-1-phosphate receptor signalling in the heart
Means, C. K., & Brown, J. H. (2008) · Cardiovascular Research · doi:10.1093/cvr/cvp086 · Cited by 238 · see citing works
Neuroglobin-overexpressing transgenic mice are resistant to cerebral and myocardial ischemia
Khan, A. A., Wang, Y., Sun, Y., Mao, X. O., Xie, L., Miles, E., Graboski, J., Chen, S., Ellerby, L., Jin, K., et al. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0607497103 · Cited by 215 · see citing works
Gestational Hypoxia and Developmental Plasticity
Ducsay, C. A., Goyal, R., Pearce, W. J., Wilson, S. M., Hu, X., & Zhang, L. (2018) · Physiological Reviews · doi:10.1152/physrev.00043.2017 · Cited by 203 · see citing works
Augmented O-GlcNAc signaling attenuates oxidative stress and calcium overload in cardiomyocytes
Ngoh, G. A., Watson, L. J., Facundo, H. T., & Jones, S. P. (2010) · Amino Acids · doi:10.1007/s00726-010-0728-7 · Cited by 180 · see citing works
Self-citationEndothelium-Derived Neuregulin Protects the Heart Against Ischemic Injury
Hedhli, N., Huang, Q., Kalinowski, A., Palmeri, M., Hu, X., Russell, R. R., & Russell, K. S. (2011) · Circulation · doi:10.1161/circulationaha.110.991125 · Cited by 173 · see citing works
Insulin says NO to cardiovascular disease
Yu, Q., Gao, F., & Ma, X. L. (2011) · Cardiovascular Research · doi:10.1093/cvr/cvq349 · Cited by 172 · see citing works
Burwell, L. S., & Brookes, P. S. (2007) · Antioxidants and Redox Signaling · doi:10.1089/ars.2007.1845 · Cited by 172 · see citing works
“The NOS-dependent protection was found to be abrogated with the administration of a commonly used NOS inhibitor, N (G)-nitro- L -arginine methyl ester (L-NAME) (39 132).”
Sansbury, B. E., Cummins, T. D., Tang, Y., Hellmann, J., Holden, C. R., Harbeson, M. A., Chen, Y., Patel, R. P., Spite, M., Bhatnagar, A., et al. (2012) · Circulation Research · doi:10.1161/circresaha.112.266395 · Cited by 156 · see citing works
The role of SIRT1 in diabetic cardiomyopathy
Karbasforooshan, H., & Karimi, G. (2017) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2017.03.056 · Cited by 155 · see citing works
Tao, J., Zhu, W. M., Li, Y., Xin, P., Li, J., Liu, M., Li, J., Redington, A. N., & Wei, M. (2011) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00097.2011 · Cited by 152 · see citing works
“While the beneficial role of eNOS against I/R injury has been well demonstrated (11, 20, 36), its role in ER stress has been controversial (13, 24, 47).”
BackgroundTsutsumi, Y. M., Horikawa, Y. T., Jennings, M., Kidd, M. W., Niesman, I. R., Yokoyama, U., Head, B. P., Hagiwara, Y., Ishikawa, Y., Miyanohara, A., et al. (2008) · Circulation · doi:10.1161/circulationaha.108.788331 · Cited by 148 · see citing works
Recent advances in the understanding of the role of nitric oxide in cardiovascular homeostasis
Schulz, R., Rassaf, T., Massion, P. B., Kelm, M., & Balligand, J. (2005) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2005.04.005 · Cited by 146 · see citing works
Samuel, S. M., Thirunavukkarasu, M., Penumathsa, S. V., Paul, D., & Maulik, N. (2008) · Journal of Agricultural and Food Chemistry · doi:10.1021/jf802050h · Cited by 133 · see citing works
SIRT1 protects against myocardial ischemia–reperfusion injury via activating eNOS in diabetic rats
Ding, M., Lei, J., Han, H.-C., Wei-bo, L., Qu, Y., Fu, E., Fu, F., & Wang, X. (2015) · Cardiovascular Diabetology · doi:10.1186/s12933-015-0299-8 · Cited by 128 · see citing works
“Activation of eNOS has been demonstrated to clearly reduce myocardial infarct size and improve cardiac function in a variety of I/R models [27, 28].”
BackgroundCOHEN, M., YANG, X., & Downey, J. M. (2005) · Cardiovascular Research · doi:10.1016/j.cardiores.2005.10.021 · Cited by 128 · see citing works
“[36] studied strains of mice overexpressing either bovine or human eNOS.”
BackgroundAragón, J. P., Condit, M. E., Bhushan, S., Predmore, B. L., Patel, S., Grinsfelder, D. B., Gundewar, S., Jha, S. K., Calvert, J. W., Barouch, L. A., et al. (2011) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2011.09.033 · Cited by 127 · see citing works
Self-citationRoy, R., Wilcox, J., Webb, A. J., & O’Gallagher, K. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242015200 · Cited by 128 · see citing works
“Furthermore, mice overexpressing eNOS have shown attenuated IRI, with beneficial effects of eNOS overexpression being reversed by the non-selective NOS inhibitor N G -nitro-L-arginine methyl ester (L-NAME) [93].”
BackgroundMoens, A. L., Champion, H. C., Claeys, M. J., Tavazzi, B., Kaminski, P. M., Wolin, M. S., Borgonjon, D. J., Nassauw, L. V., Haile, A., Zviman, M. M., et al. (2008) · Circulation · doi:10.1161/circulationaha.107.725481 · Cited by 119 · see citing works
Zhao, X., He, G., Chen, Y., Pandian, R. P., Kuppusamy, P., & Zweier, J. L. (2005) · Circulation · doi:10.1161/circulationaha.104.527226 · Cited by 117 · see citing works
Altered Nitric Oxide System in Cardiovascular and Renal Diseases
Lee, J., Bae, E. H., Kwon, S., & Kim, S. W. (2016) · Chonnam Medical Journal · doi:10.4068/cmj.2016.52.2.81 · Cited by 116 · see citing works
“Genetic overexpression of eNOS ameliorates myocardial I/R injury, which is ablated by L-NAME.(48) NO-donating compounds including L-arginine are highly beneficial in the setting of myocardial I/R injuries.”
BackgroundNitric Oxide Signaling and Regulation in the Cardiovascular System: Recent Advances
Carlström, M., Weitzberg, E., & Lundberg, J. O. (2024) · Pharmacological Reviews · doi:10.1124/pharmrev.124.001060 · Cited by 103 · see citing works
Potential novel pharmacological therapies for myocardial remodelling
Landmesser, U., Wollert, K. C., & Drexler, H. (2008) · Cardiovascular Research · doi:10.1093/cvr/cvn317 · Cited by 109 · see citing works
“concentrations protects cardiomyocytes from ischemia/reperfusion-injury via soluble guanylyl cyclase activation and cGMP formation [47-51].”
BackgroundXiao, C., Xia, M., Wang, J., Zhou, X., Lou, Y.-Y., Tang, L., Zhang, F., Yang, J.-T., & Qian, L.-B. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/2719252 · Cited by 105 · see citing works
Mitochondrial reprogramming through cardiac oxygen sensors in ischaemic heart disease
Cadenas, S., Aragonés, J., & Landázuri, M. O. (2010) · Cardiovascular Research · doi:10.1093/cvr/cvq256 · Cited by 101 · see citing works
“Conversely, transgenic mice expressing significantly more eNOS than their littermates presented a significantly smaller infarct area following IR.(116) It is thought that NO gen-”
BackgroundGene therapy for ischemic heart disease
Lavu, M., Gundewar, S., & Lefer, D. J. (2010) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2010.06.007 · Cited by 101 · see citing works
“Nitric oxide (NO) is a signaling molecule with multiple protective functions in the heart especially during I/R injury [105].”
BackgroundSelf-citationZhang, J., & Cai, H. “. (2009) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2009.11.020 · Cited by 97 · see citing works
“It has been established that a deficiency in endothelial nitric oxide synthase (eNOS) exacerbates myocardial I/R injury, whereby eNOS overexpression, NO donor, or dietary supplementation of nitrite significantly improved cardiac function in models of hypoxia and myocardial I/R injury [17-21].”
Elrod, J. W., Greer, J. J. M., Bryan, N. S., Langston, W., Szot, J. F., Gebregzlabher, H., Janssens, S. P., Feelisch, M., & Lefer, D. J. (2006) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000224324.52466.e6 · Cited by 98 · see citing works
Self-citationGuo, J., Yang, T., Sun, X. G., Zhou, N. Y., Li, F. S., Long, D., Lin, T., Li, P. Y., & Feng, L. (2011) · Journal of Biomedical Science · doi:10.1186/1423-0127-18-79 · Cited by 95 · see citing works
“NO production by eNOS seems to be of central importance in ischemic injury [38,39].”
BackgroundPachori, A. S., Melo, L. G., Hart, M. L., Noiseux, N., Zhang, L., Morello, F., Solomon, S. D., Stahl, G. L., Pratt, R. E., & Dzau, V. J. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0404616101 · Cited by 95 · see citing works
NO-Rich Diet for Lifestyle-Related Diseases
Kobayashi, J., Ohtake, K., & Uchida, H. (2015) · Nutrients · doi:10.3390/nu7064911 · Cited by 94 · see citing works
Brainard, R. E., Watson, L. J., DeMartino, A. M., Brittian, K. R., Readnower, R. D., Boakye, A. A., Zhang, D., Hoetker, J. D., Bhatnagar, A., Baba, S. P., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0083174 · Cited by 93 · see citing works
“Myocardial Ischemia/Reperfusion (MI-R) Studies: Threemonth-old male db/db mice and their heterozygous littermates were subjected to in vivo coronary artery ischemia–reperfusion as previously described [13,15,18-26].”
MethodSelf-citationGenetic overexpression of eNOS attenuates hepatic ischemia-reperfusion injury
Duranski, M. R., Elrod, J. W., Calvert, J. W., Bryan, N. S., Feelisch, M., & Lefer, D. J. (2006) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01173.2005 · Cited by 88 · see citing works
Self-citationWood, K. C., Hebbel, R. P., Lefer, D. J., & Granger, D. N. (2006) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2005.12.015 · Cited by 86 · see citing works
Self-citationDiesen, D. L., & Kuo, P. C. (2009) · Journal of Surgical Research · doi:10.1016/j.jss.2009.10.006 · Cited by 84 · see citing works
“Genetic overexpression of eNOS also attenuates hepatic ischemia/reperfusion injury as compared to control mice [26,72].”
BackgroundMyocardial protection by nitrite
Calvert, J. W., & Lefer, D. J. (2009) · Cardiovascular Research · doi:10.1093/cvr/cvp079 · Cited by 82 · see citing works
Legrand, M. M., Almac, E., Mik, E. G., Johannes, T., Kandil, A., Bezemer, R., Payen, D. M., & İnce, C. (2009) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.90371.2008 · Cited by 82 · see citing works
Chiari, P. C., Bienengraeber, M. W., Weihrauch, D., Krolikowski, J. G., Kersten, J. R., Warltier, D. C., & Pagel, P. S. (2005) · Anesthesiology · doi:10.1097/00000542-200507000-00014 · Cited by 79 · see citing works
“Overexpression of eNOS also attenuated myocardial ischemia– reperfusion injury in transgenic mice.(36,37) Increases in iNOS mRNA transcription were observed in rat myocardium after infarction but not hypoxia–reoxygenation.”
BackgroundClinical Implications of Apoptosis in Ischemic Myocardium
Scarabelli, T. M., Knight, R. A., Stephanou, A., Townsend, P. A., Chen-Scarabelli, C. A., Lawrence, K. M., Gottlieb, R. A., Latchman, D. S., & Narula, J. (2006) · Current Problems in Cardiology · doi:10.1016/j.cpcardiol.2005.11.002 · Cited by 76 · see citing works
eNOS Gene Therapy Exacerbates Hepatic Ischemia-Reperfusion Injury in Diabetes
Elrod, J. W., Duranski, M. R., Langston, W., Greer, J. J. M., Tao, L., Dugas, T. R., Kevil, C. G., Champion, H. C., & Lefer, D. J. (2006) · Circulation Research · doi:10.1161/01.res.0000231306.03510.77 · Cited by 75 · see citing works
Self-citationClinical translation of nitrite therapy for cardiovascular diseases
Calvert, J. W., & Lefer, D. J. (2010) · Nitric Oxide · doi:10.1016/j.niox.2009.11.001 · Cited by 72 · see citing works
“I/R injury [24,25], whereas the overexpression of eNOS [26,27], the administration of NO donors [28–32] and inhaled NO gas therapy [33] are all cytoprotective [34].”
BackgroundSelf-citationМаслов, Л. Н., IuB, L., Oeltgen, P. R., Barzakh, E. I., Krylatov, A. V., Govindaswami, M., & Brown, S. A. (2009) · Life Sciences · doi:10.1016/j.lfs.2009.02.016 · Cited by 72 · see citing works
Adluri, R. S., Thirunavukkarasu, M., Dunna, N. R., Zhan, L., Oriowo, B., Takeda, K., Sánchez, J. A., Otani, H., Maulik, G., Fong, G., et al. (2010) · Antioxidants and Redox Signaling · doi:10.1089/ars.2010.3769 · Cited by 73 · see citing works
“Further, nitric oxide (NO) produced by eNOS is a signaling molecule with multiple protective functions in the heart especially during I/R injury (11).”
Role of Oxygen in Postischemic Myocardial Injury
Kutala, V. K., Khan, M., Angelos, M. G., & Kuppusamy, P. (2007) · Antioxidants and Redox Signaling · doi:10.1089/ars.2007.1636 · Cited by 66 · see citing works
“However, NO has also been shown to play a cardioprotective role in myocardial IR injury (63, 80, 115, 131, 138, 158).”
Yamagata, K., & Yamori, Y. (2019) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000000757 · Cited by 64 · see citing works
Shen, M., Wang, L., Yang, G., Gao, L., Wang, B., Guo, X., Zeng, C., Xu, Y., Shen, L., Cheng, K., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0088389 · Cited by 63 · see citing works
“Endothelial nitric oxide synthase (eNOS) is an essential cell protective mediator under multiple conditions [11,25].”
BackgroundWang, Q., Donthi, R. V., Wang, J., Lange, A. J., Watson, L. J., Jones, S. P., & Epstein, P. N. (2008) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.91501.2007 · Cited by 63 · see citing works
Self-citationAmour, J., Brzezinska, A. K., Weihrauch, D., Billstrom, A. R., Zielonka, J., Krolikowski, J. G., Bienengraeber, M. W., Warltier, D. C., Pratt, P. F., & Kersten, J. R. (2009) · Anesthesiology · doi:10.1097/aln.0b013e3181942cb4 · Cited by 62 · see citing works
“Myocardial ischemia and reperfusion injury is attenuated in mice with myocyte-specific overexpression of eNOS(38) and infarct size is reduced in transgenic mice overexpressing either bovine or human eNOS.(39) Conversely, myocardial infarct size is markedly increased in eNOS knockout mice.”
BackgroundEmergent role of gasotransmitters in ischemia-reperfusion injury
Moody, B. F., & Calvert, J. W. (2011) · Medical Gas Research · doi:10.1186/2045-9912-1-3 · Cited by 61 · see citing works
“Early studies reported that a deficiency of nNOS or iNOS did not affect infarct size in response to acute myocardial ischemia [24,28, 30-32 ].”
BackgroundZhang, Y., Huang, Y., Cantalupo, A., Azevedo, P. S., Siragusa, M., Bielawski, J., Giordano, F. J., & Lorenzo, A. D. (2016) · JCI Insight · doi:10.1172/jci.insight.85484 · Cited by 61 · see citing works
“In the long term (3 months after surgery), Nogo-A/B–deficient mice were also protected from fibrosis, cardiac remodeling, and dysfunction, probably by different means: (a) indirectly, due to reduced myocardial permeability, inflammation, and fibrosis; (b) by hyperactivation of the S1P/eNOS/NO pathway (18) and, thus, i…”
BackgroundLemoine, S., Tritapepe, L., Hanouz, J., & Puddu, P. E. (2016) · British Journal of Anaesthesia · doi:10.1093/bja/aev451 · Cited by 59 · see citing works
Production of endothelial nitric oxide synthase (eNOS) over-expressing piglets
Hao, Y., Yong, H. Y., Murphy, C. N., Wax, D., Samuel, M., Rieke, A., Lai, L., Liu, Z., Durtschi, D. C., Welbern, V., et al. (2006) · Transgenic Research · doi:10.1007/s11248-006-9020-8 · Cited by 60 · see citing works
Designing Heart Performance by Gene Transfer
Davis, J., Westfall, M. V., Townsend, D., Blankinship, M. J., Herron, T. J., Guerrero‐Serna, G., Wang, W., Devaney, E. J., & Metzger, J. M. (2008) · Physiological Reviews · doi:10.1152/physrev.00039.2007 · Cited by 58 · see citing works
“Some of this beneficial effect may be related to NOS3 effects on cardiac-associated neural and endothelial compartments (253, 415, 440, 441, 776).”
BackgroundSu, W., Zhang, Y., Zhang, Q., Xu, J., Zhan, L., Zhu, Q., Lian, Q., Liu, H., Xia, Z., Xia, Z., et al. (2016) · Cardiovascular Diabetology · doi:10.1186/s12933-016-0460-z · Cited by 60 · see citing works
“The eNOSderived NO has been reported to inhibit the progression of myocardial infarction [8], ameliorate myocardial I/R injury [9] and left ventricular hypertrophy [10, 11], and prevent the onset of heart failure [12].”
BackgroundShao, Z., Wojcik, K. R., Dossumbekova, A., Hsu, C., Mehendale, S. R., Li, C., Qin, Y., Sharp, W. W., Chang, W., Hamann, K. J., et al. (2009) · Journal of Cellular Biochemistry · doi:10.1002/jcb.22170 · Cited by 58 · see citing works
“In addition, eNOS over-expression induced in endothelial tissue improved reperfusion injury in a transgenic mouse model [Jones et al., 2004], underlining the fact that enzymatic NO attenuates reperfusion injury.”
Mustafa, H. N., Hegazy, G. A., Awdan, S. A. E., & Elbaset, M. A. (2017) · Tissue and Cell · doi:10.1016/j.tice.2017.03.007 · Cited by 59 · see citing works
Yang, J.-T., Qian, L.-B., Zhang, F., Wang, J., Ai, H., Tang, L., & Wang, H. (2014) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0000000000000202 · Cited by 58 · see citing works
“In addition, some additional systemic effects (eg, altering the bioavailability of other compounds) of luteolin in vivo needs to be addressed in future studies because it has been revealed that plant extracts with a high diversity of polyphenol compounds (eg, luteolin and apigenin) may have higher bioavailability than…”
MethodInfluentialPenumathsa, S. V., Koneru, S., Thirunavukkarasu, M., Zhan, L., Prasad, K., & Maulik, N. (2006) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.106.114165 · Cited by 57 · see citing works
“, 1999) showed that in eNOS-deficient mice infarct size was significantly augmented and in eNOS transgenic mice infarct size was reduced after ischemia and reperfusion, supporting the role of eNOS-derived NO during I/R injury and cardioprotection (Jones et al., 2004).”
BackgroundBurkard, N., Williams, T., Czolbe, M., Blömer, N., Panther, F., Link, M., Fraccarollo, D., Widder, J. D., Hu, K., Han, H. J., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.933630 · Cited by 56 · see citing works
Redox Signaling Pathways Involved in Neuronal Ischemic Preconditioning
Thompson, J. W., Narayanan, S. V., & Perez-Pinzon, M. (2012) · Current Neuropharmacology · doi:10.2174/157015912804143577 · Cited by 70 · see citing works
“Mice overexpressing eNOS had reduced infarct size when compared to wild type littermates following cardiac ischemia [51], suggesting that NO plays an important role in protective signaling following oxidative stress.”
Nitric Oxide in the Pathogenesis of Cardiac Disease
Raij, L. R. (2006) · Journal of Clinical Hypertension · doi:10.1111/j.1524-6175.2006.06025.x · Cited by 54 · see citing works
Redox Signaling Pathways Involved in Neuronal Ischemic Preconditioning
Thompson, J. W., Narayanan, S., & Pérez‐Pinzón, M. A. (2012) · Current Neuropharmacology · doi:10.2174/157015912804499519 · Cited by 49 · see citing works
Molecular Mechanisms Underlying Heart Failure and Their Therapeutic Potential
Fonseka, O., Gare, S. R., Chen, X., Zhang, J., Alatawi, N. H. O., Ross, C., & Liu, W. (2025) · Cells · doi:10.3390/cells14050324 · Cited by 50 · see citing works
Oidor-Chan, V. H., Hong, E., Pérez‐Severiano, F., Montes, S., Torres-Narváez, J. C., del Valle‐Mondragón, L., Pastelín-Hernández, G. S., & Sánchez-Mendoza, A. (2016) · PPAR Research · doi:10.1155/2016/8237264 · Cited by 46 · see citing works
“Further, numerous studies have demonstrated cardioprotective effects of NO during I/R in T2D and nondiabetic models [8, 36, 37].”
BackgroundNitrite and myocardial ischaemia reperfusion injury. Where are we now?
Griffiths, K., Lee, J. J., Frenneaux, M. P., Feelisch, M., & Madhani, M. (2021) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2021.107819 · Cited by 46 · see citing works
Penumathsa, S. V., Koneru, S., Zhan, L., John, S., Menon, V. P., Prasad, K., & Maulik, N. (2007) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2007.09.014 · Cited by 46 · see citing works
“Several other studies (34) have shown that infarct size was significantly augmented in eNOS deficient mice, and infarct size was reduced in eNOS transgenic mice following ischemia and reperfusion, thus supporting the role of eNOS-derived NO during ischemia–reperfusion injury and cardioprotection (35).”
BackgroundClass II transactivator (CIITA) mediates IFN-γ induced eNOS repression by enlisting SUV39H1
Weng, X., Zhang, Y., Li, Z., Yu, L., Xu, F., Fang, M., Hou, L., Ge, J., & Xu, Y. (2019) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2019.01.005 · Cited by 45 · see citing works
Cook, S. (2006) · Swiss Medical Weekly · doi:10.4414/smw.2006.11068 · Cited by 45 · see citing works
Gonon, A. T., Erbaş, D., Bröijersén, A., Valen, G., & Pernow, J. (2004) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00544.2003 · Cited by 45 · see citing works
“This observation may be of interest considering that hearts from eNOS transgenic mice are protected against ischemia and reperfusion injury (6, 15).”
BackgroundSomarathna, M. S., Hwang, P. T. J., Millican, R. C., Alexander, G. C., Waldrop, T. I., Sherwood, J. A., Brott, B. C., Falzon, I. D., Northrup, H. M., Shiu, Y.-T. E., et al. (2021) · Biomaterials · doi:10.1016/j.biomaterials.2021.121254 · Cited by 44 · see citing works
Pattillo, C. B., Bir, S. C., Rajaram, V., & Kevil, C. G. (2010) · Cardiovascular Research · doi:10.1093/cvr/cvq297 · Cited by 43 · see citing works
A Metabolomic Study of Rats with Doxorubicin-Induced Cardiomyopathy and Shengmai Injection Treatment
Chen, Y., Tang, Y. M., Zhang, Y.-C., Huang, X.-H., Xie, Y.-Q., & Yin, X. (2015) · PLoS ONE · doi:10.1371/journal.pone.0125209 · Cited by 43 · see citing works
“effects, including the inhibition of oxidative stress [40,41].”
BackgroundKhan, M., Mohan, I. K., Kutala, V. K., Kotha, S. R., Parinandi, N. L., Hamlin, R. L., & Kuppusamy, P. (2008) · Antioxidants and Redox Signaling · doi:10.1089/ars.2008.2155 · Cited by 43 · see citing works
“However, NO has also been shown to play a cardioprotective role in myocardial I=R injury (28, 36, 48, 54, 57, 63).”
Talukder, M. A. H., Yang, F., Shimokawa, H., & Zweier, J. L. (2010) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00384.2010 · Cited by 43 · see citing works
Relevance of nitric oxide for myocardial remodeling
Massion, P. B., & Balligand, J. (2007) · Current Heart Failure Reports · doi:10.1007/s11897-007-0021-6 · Cited by 42 · see citing works
“Endothelial-restricted eNOS overexpression afforded protection with reduced MI and better diastolic function at day 7 after reperfusion compared with nontransgenic mice [ 62 ].”
BackgroundA New Method to Stabilize C-Kit Expression in Reparative Cardiac Mesenchymal Cells
Wysoczynski, M., Dassanayaka, S., Zafir, A., Ghafghazi, S., Long, B. W., Noble, C. T., DeMartino, A. M., Brittian, K. R., Bolli, R., & Jones, S. P. (2016) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2016.00078 · Cited by 41 · see citing works
Self-citationThe eNOS enhancer AVE 9488: a novel cardioprotectant against ischemia reperfusion injury
Frantz, S., Adamek, A., Fraccarollo, D., Tillmanns, J., Widder, J. D., Dienesch, C., Schäfer, A., Podolskaya, A. A., Held, M. C., Ruetten, H., et al. (2009) · Basic Research in Cardiology · doi:10.1007/s00395-009-0041-3 · Cited by 41 · see citing works
“Indeed, mice overexpressing eNOS had reduced infarct sizes after ischemia/ reperfusion injury [22].”
BackgroundGross, G. J., Hsu, A., Pfeiffer, A. W., & Nithipatikom, K. (2013) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2013.02.003 · Cited by 40 · see citing works
“NO derived from eNOS has been demonstrated to posses cardioprotective effects not only against acute ischemia/reperfusion [25,26,44,45] but also are involved in early ischemic preconditioning [45] as well as a late phase of ischemic preconditioning [46].”
Ahmed, S. M., Abdelrahman, S. A., & Salama, A. E. (2017) · Ultrastructural Pathology · doi:10.1080/01913123.2017.1281367 · Cited by 39 · see citing works
“eNOs is expressed in cardiac myocytes, conduction tissue, and the endothelium [7].”
BackgroundHansell, J. A., Richter, H. G., Camm, E. J., Herrera, E. A., Blanco, C. E., Villamor, E., Patey, O. V., Lock, M. C., Trafford, A. W., Galli, G. L. J., et al. (2021) · Journal of Pineal Research · doi:10.1111/jpi.12766 · Cited by 39 · see citing works
PKA-mediated eNOS phosphorylation in the protection of ischemic preconditioning against no-reflow
Li, X., Cheng, Y., Yang, Y.-J., Meng, X., Zhao, J., Zhang, H., Wu, Y., You, S.-J., & Wu, Y. (2012) · Microvascular Research · doi:10.1016/j.mvr.2012.04.002 · Cited by 39 · see citing works
Discoveries of Hydrogen Sulfide as a Novel Cardiovascular Therapeutic
Barr, L. A., & Calvert, J. W. (2014) · Circulation Journal · doi:10.1253/circj.cj-14-0728 · Cited by 37 · see citing works
Hirata, K., Maruyama, T., Watanabe, H., Maeda, H., Nakajou, K., Iwao, Y., Ishima, Y., Katsumi, H., Hashida, M., & Otagiri, M. (2010) · Journal of Controlled Release · doi:10.1016/j.jconrel.2010.03.010 · Cited by 37 · see citing works
Nishida, T., Yu, J., Minamishima, S., Sips, P. Y., Searles, R. J., Buys, E. S., Janssens, S. P., Brouckaert, P., Bloch, K. D., & Ichinose, F. (2008) · Critical Care Medicine · doi:10.1097/ccm.0b013e318192face · Cited by 36 · see citing works
“For instance, overexpression of NOS3 in endothelial cells (5) or cardiomyocytes (6) attenuates IR injury in the heart, whereas NOS3 deficiency has been reported to exacerbate IR-induced myocardial stunning (7).”
BackgroundCalvert, J. W., Gundewar, S., Yamakuchi, M., Park, P. C., Baldwin, W. M., Lefer, D. J., & Lowenstein, C. J. (2007) · Circulation Research · doi:10.1161/circresaha.107.162610 · Cited by 35 · see citing works
Self-citationBhushan, S., Kondo, K., Predmore, B. L., Zlatopolsky, M., King, A. L., Pearce, C., Huang, H., Tao, Y., Condit, M. E., & Lefer, D. J. (2012) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.112.251769 · Cited by 35 · see citing works
Self-citationPGE1analog alprostadil induces VEGF and eNOS expression in endothelial cells
Haider, D. G., Bucek, R. A., Giurgea, A., Maurer, G., Glogar, H. D., Minar, E., Wolzt, M., Mehrabi, M. R., & Baghestanian, M. (2005) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00147.2005 · Cited by 35 · see citing works
“Targeted eNOS overexpression attenuates cardiac and endothelial dysfunction and dramatically improves survival in severe HF (13, 14).”
BackgroundCardioprotective actions of nitrite therapy and dietary considerations
Nathan, S. B. (2009) · Frontiers in bioscience · doi:10.2741/3568 · Cited by 34 · see citing works
“Previous studies clearly demonstrate that the deficiency of eNOS exacerbates myocardial I/R injury (8, 9), whereas the overexpression of eNOS (10, 11), NO donor (12, 13) or inhaled NO gas (14) therapy significantly protect the myocardium (15).”
BackgroundMajumder, S., Sinha, S., Siamwala, J. H., Muley, A., Seerapu, H. R., Kolluru, G. K., Veeriah, V., Nagarajan, S., Sridhara, S. R. C., Priya, M. K., et al. (2013) · Nitric Oxide · doi:10.1016/j.niox.2013.12.002 · Cited by 34 · see citing works
Placental Growth Factor Influences Maternal Cardiovascular Adaptation to Pregnancy in Mice1
Aasa, K. L., Zavan, B., Luna, R. L., Wong, P. G., Ventura, N. M., Tse, M. Y., Carmeliet, P., Adams, M. A., Pang, S. C.-N., & Croy, B. A. (2014) · Biology of Reproduction · doi:10.1095/biolreprod.114.124677 · Cited by 33 · see citing works
“Members of the NOS gene system are prominent amongst the genes altered during cardiac stress and, like PGF, participate in cardioprotection, the hypertrophic response, and angiogenesis [34, 36, 38, 39].”
BackgroundMyocardial injury: where inflammation and autophagy meet
Liu, C., Liu, Y., Chen, H., Yang, X., Lu, C., Wang, L., & Lu, J. (2023) · Burns & Trauma · doi:10.1093/burnst/tkac062 · Cited by 33 · see citing works
“eNOS participates in the protective role of ischemia postadaptation [79].”
Sphingolipid Metabolism and Signaling in Endothelial Cell Functions
Sasset, L., & Lorenzo, A. D. (2022) · Advances in experimental medicine and biology · doi:10.1007/978-981-19-0394-6_8 · Cited by 32 · see citing works
- Authors
- Jones, S. P., Greer, J. J. M., Kakkar, A. K., Ware, P. D., Turnage, R. H., Hicks, M., van Haperen, R., de Crom, R., Kawashima, S., Yokoyama, M., & Lefer, D. J.
- Affiliations
- Louisiana State University Health Sciences Center Shreveport (US)
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2004-01
- Volume
- 286
- Issue
- 1
- Pages
- H276-H282
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2133542546
- Cited by
- 206
- References
- 37
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 8 · 2020: 1 · 2019: 6 · 2018: 8 · 2017: 12 · 2016: 10 · 2015: 9 · 2014: 14 · 2013: 6 · 2012: 13
- FWCI
- 9.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL60849, R01HL060849)
- National Institute of Diabetes and Digestive and Kidney Diseases (P01 DK-43785, P01DK043785)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
- Keywords
- endothelial nitric oxide synthase, myocardial ischemia-reperfusion injury, myocardial infarct size, nitric oxide, transgenic mice, left ventricular end-diastolic pressure, L-NAME, cardioprotection
- MeSH terms
- Alkenes, Animals, Cattle, Decanoic Acids, Echocardiography, Heart, Hemodynamics, Humans, Hydroxy Acids, Mice, Inbred Strains, Mice, Transgenic, Myocardial Infarction, Myocardium, Time Factors, Myocardial Reperfusion Injury, Myocardial Ischemia, Nitric Oxide Synthase, Nitric Oxide Donors, Mice, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III
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