Reactivity of renal and mesenteric resistance vessels to angiotensin II is mediated by NOXA1/NOX1 and superoxide signaling

Stevenson, Mark D.; Vendrov, Aleksandr E.; Yang, Xi; Chen, Yuenmu; Navarro, Hernán A.; Moss, Nicholas; Runge, Marschall S.; Arendshorst, William J.; Madamanchi, Nageswara R.

doi:10.1152/ajprenal.00236.2022

Cited by 8

The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.

Reactivity of renal and mesenteric resistance vessels to angiotensin II is mediated by NOXA1/NOX1 and superoxide signaling

Stevenson, Mark D., Vendrov, Aleksandr E., Yang, Xi, Chen, Yuenmu, Navarro, Hernán A., Moss, Nicholas, Runge, Marschall S., Arendshorst, William J., Madamanchi, Nageswara R.·2023·American Journal of Physiology-Renal Physiology

DOI 10.1152/ajprenal.00236.2022

Open this paper in CoChat — free account

Abstract

Renal reactivity to angiotensin II (ANG II) is mediated by superoxide signaling produced by NADPH oxidase (NOX)A1/NOX1. Acute vasoconstriction of renal arteries by ANG was blunted in Noxa1−/− compared with wild-type mice. NOXA1/NOX1/O 2•− signaling was also observed in ANG II stimulation of vascular smooth muscle cells and isolated mesenteric resistance arteries, indicating that it contributes to ANG II-induced hypertension. A NOXA1/NOX1 assembly inhibitor (C25) has been characterized that inhibits superoxide production and ameliorates the effects of ANG II.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1152/ajprenal.00236.2022

Cites

7 of 7 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

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?

Vascular reactivity was assessed by wire myography as previously described.
“Vascular reactivity assessed by wire myography was performed as previously described [83].”
From Genetic variation in CCDC93 is associated with elevated central systolic blood pressure, impaired arterial relaxation, and mitochondrial dysfunction (2024) · cites this paper as [83]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Novel gp91 phox Homologues in Vascular Smooth Muscle Cells: nox1 Mediates Angiotensin II–Induced Superoxide Formation and Redox-Sensitive Signaling Pathways
Lassègue, B., Sorescu, D., Szöcs, K., Yin, Q., Akers, M., Zhang, Y., Grant, S. L., Lambeth, J. D., & Griendling, K. K. (2001) · Circulation Research · doi:10.1161/hh0901.090299 · Cited by 839
Effects of Angiotensin II Infusion on the Expression and Function of NAD(P)H Oxidase and Components of Nitric Oxide/cGMP Signaling
Mollnau, H., Wendt, M., Szöcs, K., Lassègue, B., Schulz, E., Oelze, M., Li, H., Bodenschatz, M., August, M., Kleschyov, A. L., et al. (2002) · Circulation Research · doi:10.1161/01.res.0000012569.55432.02 · Cited by 676
A gp91phox Containing NADPH Oxidase Selectively Expressed in Endothelial Cells Is a Major Source of Oxygen Radical Generation in the Arterial Wall
Görlach, A., Brandes, R. P., Nguyen, K., Amidi, M., Dehghani, F., & Busse, R. (2000) · Circulation Research · doi:10.1161/01.res.87.1.26 · Cited by 598
Nox1 Is Involved in Angiotensin II–Mediated Hypertension: A Study in Nox1-Deficient Mice
Matsuno, K., Yamada, H., Iwata, K., Jin, D., Katsuyama, M., Matsuki, M., Takai, S., Yamanishi, K., Miyazaki, M., Matsubara, H., et al. (2005) · Circulation · doi:10.1161/circulationaha.105.573709 · Cited by 470
Nox1 Overexpression Potentiates Angiotensin II-Induced Hypertension and Vascular Smooth Muscle Hypertrophy in Transgenic Mice
Dikalova, A., Clempus, R., Lassègue, B., Cheng, G., McCoy, J., Dikalov, S., Martin, A. S., Lyle, A., Weber, D. S., Weiss, D., et al. (2005) · Circulation · doi:10.1161/circulationaha.105.538934 · Cited by 438
A Mouse Model of Angiotensin II Slow Pressor Response: Role of Oxidative Stress
Kawada, N., Imai, E., Karber, A., Welch, W. J., & Wilcox, C. S. (2002) · Journal of the American Society of Nephrology · doi:10.1097/01.asn.0000035087.11758.ed · Cited by 195
Upregulation of nox1 in vascular smooth muscle leads to impaired endothelium-dependent relaxation via enos uncoupling
Dikalova, A. E., Góngora, M. C., Harrison, D. G., Lambeth, J. D., Dikalov, S., & Griendling, K. K. (2010) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00242.2010 · Cited by 179

Flagged first, then by citations

Research works printed but not linked: 103

10.1161/01.CIR.0000105680.92873.70 · DOI · Paper page
10.1038/hr.2010.201 · DOI
10.3390/antiox10060890 · DOI · Paper page
10.1172/JCI65460 · DOI
10.1089/ars.2021.0047 · DOI
10.1152/ajprenal.2000.279.2.F319 · DOI
10.1161/HYPERTENSIONAHA.109.133785 · DOI
10.1161/01.HYP.0000200027.34925.93 · DOI
10.1097/00004872-200207000-00025 · DOI
10.3389/fphys.2020.566410 · DOI
10.1089/152308602762197443 · DOI
10.1152/ajprenal.00060.2004 · DOI
10.1089/ars.2013.5259 · DOI
10.1159/000110021 · DOI
10.1161/01.RES.0000057755.02845.F9 · DOI
10.1046/j.0001-6772.2003.01204.x · DOI
10.1161/01.hyp.33.1.424 · DOI
10.1291/hypres.29.813 · DOI
10.1016/s0891-5849(01)00727-4 · DOI
10.1152/ajpregu.00476.2002 · DOI
10.1161/HYPERTENSIONAHA.115.06280 · DOI
10.1007/s00395-011-0179-7 · DOI
10.1152/ajprenal.00427.2016 · DOI
10.1152/ajprenal.00152.2017 · DOI
10.1152/ajprenal.00107.2022 · DOI
10.1152/ajpheart.00715.2006 · DOI
10.1152/ajprenal.00506.2007 · DOI
10.1152/ajprenal.00048.2013 · DOI
10.1161/HYPERTENSIONAHA.111.184291 · DOI
10.1161/01.HYP.0000111137.15873.4a · DOI
10.1159/000108758 · DOI
10.1038/sj.bjp.0705557 · DOI
10.1006/jmcc.2000.1134 · DOI
10.1097/00005344-199904000-00013 · DOI
10.1152/ajprenal.00423.2003 · DOI
10.1152/ajpheart.01135.2010 · DOI
10.1152/ajprenal.2000.279.2.F302 · DOI
10.1111/j.1472-8206.2000.tb00387.x · DOI
10.2337/diabetes.55.01.06.db05-0831 · DOI
10.1097/00005344-199204002-00053 · DOI
10.1016/j.redox.2018.11.021 · DOI
10.1152/ajprenal.00079.2009 · DOI
10.1161/HYPERTENSIONAHA.114.04147 · DOI
10.1161/CIRCULATIONAHA.109.908319 · DOI
10.1016/j.freeradbiomed.2005.12.035 · DOI
10.1161/JAHA.117.006775 · DOI
10.1007/978-1-4939-9424-3_14 · DOI
10.1177/1087057109352902 · DOI
10.1016/j.freeradbiomed.2007.04.022 · DOI
10.1371/journal.pone.0010478 · DOI
Arendshorst WJ, 2016, Diseases of the Kidney and Urinary Tract, 74
10.1097/01.asn.0000108523.02100.e0 · DOI
10.1016/j.freeradbiomed.2015.02.009 · DOI
10.1152/ajprenal.00090.2005 · DOI
10.1038/srep42717 · DOI · Paper page
10.1073/pnas.1514161113 · DOI
10.1371/journal.pone.0111117 · DOI
Granger JP, 2000, Semin Nephrol, 20, 417
10.1152/ajprenal.1985.249.2.F299 · DOI
10.1016/j.freeradbiomed.2006.04.024 · DOI
10.1161/01.res.74.6.1141 · DOI · Paper page
10.1089/ars.2009.2584 · DOI
10.1016/j.brainres.2009.06.056 · DOI
10.1152/ajprenal.00144.2005 · DOI
10.1161/HYPERTENSIONAHA.115.05274 · DOI
10.1152/ajprenal.00575.2015 · DOI
10.1152/ajprenal.1996.270.3.F398 · DOI
10.1111/j.1365-201X.2004.01314.x · DOI
10.1152/ajprenal.00187.2015 · DOI
10.1152/ajprenal.00510.2006 · DOI
10.1038/sj.bjp.0705626 · DOI
10.1016/j.plefa.2008.01.008 · DOI
10.1586/14779072.1.1.91 · DOI
10.1161/01.HYP.0000138070.47616.9d · DOI
10.1161/01.RES.0000092140.81594.A8 · DOI · Paper page
10.1152/ajpregu.90843.2008 · DOI
10.1007/s00424-014-1548-5 · DOI
10.1038/ki.1996.256 · DOI
10.1152/ajpregu.00207.2005 · DOI
10.1152/ajpregu.1996.270.6.R1203 · DOI
10.1042/BJ20011178 · DOI
10.1152/ajprenal.00420.2006 · DOI
10.1152/ajpregu.00481.2007 · DOI
10.1161/01.hyp.27.5.1173 · DOI
10.1161/01.hyp.31.1.283 · DOI
10.1038/sj.bjp.0702090 · DOI
10.1111/j.1440-1681.2005.04203.x · DOI
10.1152/ajpregu.00482.2007 · DOI
10.1254/jjp.66.457 · DOI
10.1152/ajprenal.2000.278.2.F302 · DOI
10.1161/HYPERTENSIONAHA.110.159301 · DOI
10.1111/j.1365-201X.2004.01316.x · DOI
10.1016/s0014-2999(01)01349-8 · DOI
10.1111/j.1476-5381.1993.tb13798.x · DOI
10.1111/j.1469-7793.1998.199br.x · DOI
10.1111/j.1476-5381.2009.00396.x · DOI
10.1093/cvr/cvy023 · DOI
10.1016/j.clinre.2018.10.004 · DOI
10.1038/sj.bjp.0703052 · DOI
10.1016/j.redox.2017.11.014 · DOI
10.1161/01.hyp.18.5_suppl.iii76 · DOI
10.1096/fasebj.3.9.2545495 · DOI
10.1152/ajpheart.00969.2004 · DOI

Sorted by citations

Genetic variation in CCDC93 is associated with elevated central systolic blood pressure, impaired arterial relaxation, and mitochondrial dysfunction
Kumar, N., Yang, M.-L., Sun, P., Hunker, K. L., Li, J., Jia, J., Fan, F., Wang, J., Ning, X., Gao, W., et al. (2024) · PLOS Genetics · doi:10.1371/journal.pgen.1011151 · Cited by 1
Self-citation

Authors: Stevenson, M. D., Vendrov, A. E., Yang, X., Chen, Y., Navarro, H. A., Moss, N., Runge, M. S., Arendshorst, W. J., & Madamanchi, N. R.
Affiliations: Division of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, United States
Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, North Carolina, United States
McAllister Heart Institute, Division of Cardiology, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina, United States
Center for Drug Discovery, Organic and Medicinal Chemistry, RTI International, Research Triangle Park, North Carolina, United States
ORCID: Vendrov, Aleksandr E.
Runge, Marschall S.
Madamanchi, Nageswara R.
Venue: American Journal of Physiology-Renal Physiology
Publisher: American Physiological Society
Published: 2023-04-01
Volume: 324
Issue: 4
Pages: F335-F352
ISSN: 1931-857X
1522-1466
DOI: 10.1152/ajprenal.00236.2022
Cited by: 8
References: 7
Language: en
Funders: HHS | NIH | National Heart, Lung, and Blood Institute (HL139842)

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

Reactivity of renal and mesenteric resistance vessels to angiotensin II is mediated by NOXA1/NOX1 and superoxide signaling

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Metadata

Record

About these checks