Evidence map›Paper›PMID 26315714›Full record

ReviewPharmacological reviews2015

International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli [corrected].

Sadashiva S Karnik, Hamiyet Unal, Jacqueline R Kemp, Kalyan C Tirupula, Satoru Eguchi, Patrick M L Vanderheyden, Walter G Thomas

Erratum issuedOpen access · bronzeAbstract readReview
In one paragraph

Review in Pharmacological reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 158 papers.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed
15.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

158 citing papers in PubMed, 288 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Activation of the angiotensin II type I receptor by a nonpeptide agonist.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Review
  7. Article
  8. Review
  9. Identification ofFrontiers in pharmacology · 2026
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Deletion of ATAmerican journal of physiology. Renal physiology · 2024
    Article

98 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Sadashiva S KarnikDepartment of Molecular Cardiology, Lerner Research Institute of Cleveland Clinic, Cleveland, Ohio (S.S.K., H.U., J.R.K., K.C.T.); Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania (S.E.); Faculty of Sciences and Bioengineering Sciences, Vrije Universiteit Brussel, Brussels, Belgium (P.M.L.V.); and Department of General Physiology, School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia (W.G.T.) karniks@ccf.org.
Hamiyet UnalDepartment of Molecular Cardiology, Lerner Research Institute of Cleveland Clinic, Cleveland, Ohio (S.S.K., H.U., J.R.K., K.C.T.); Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania (S.E.); Faculty of Sciences and Bioengineering Sciences, Vrije Universiteit Brussel, Brussels, Belgium (P.M.L.V.); and Department of General Physiology, School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia (W.G.T.).
Jacqueline R KempDepartment of Molecular Cardiology, Lerner Research Institute of Cleveland Clinic, Cleveland, Ohio (S.S.K., H.U., J.R.K., K.C.T.); Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania (S.E.); Faculty of Sciences and Bioengineering Sciences, Vrije Universiteit Brussel, Brussels, Belgium (P.M.L.V.); and Department of General Physiology, School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia (W.G.T.).
Kalyan C TirupulaDepartment of Molecular Cardiology, Lerner Research Institute of Cleveland Clinic, Cleveland, Ohio (S.S.K., H.U., J.R.K., K.C.T.); Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania (S.E.); Faculty of Sciences and Bioengineering Sciences, Vrije Universiteit Brussel, Brussels, Belgium (P.M.L.V.); and Department of General Physiology, School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia (W.G.T.).
Satoru EguchiDepartment of Molecular Cardiology, Lerner Research Institute of Cleveland Clinic, Cleveland, Ohio (S.S.K., H.U., J.R.K., K.C.T.); Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania (S.E.); Faculty of Sciences and Bioengineering Sciences, Vrije Universiteit Brussel, Brussels, Belgium (P.M.L.V.); and Department of General Physiology, School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia (W.G.T.).
Patrick M L VanderheydenDepartment of Molecular Cardiology, Lerner Research Institute of Cleveland Clinic, Cleveland, Ohio (S.S.K., H.U., J.R.K., K.C.T.); Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania (S.E.); Faculty of Sciences and Bioengineering Sciences, Vrije Universiteit Brussel, Brussels, Belgium (P.M.L.V.); and Department of General Physiology, School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia (W.G.T.).
Walter G ThomasDepartment of Molecular Cardiology, Lerner Research Institute of Cleveland Clinic, Cleveland, Ohio (S.S.K., H.U., J.R.K., K.C.T.); Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania (S.E.); Faculty of Sciences and Bioengineering Sciences, Vrije Universiteit Brussel, Brussels, Belgium (P.M.L.V.); and Department of General Physiology, School of Biomedical Sciences, The University of Queensland, Brisbane, Queensland, Australia (W.G.T.).
Temple University · USVrije Universiteit Brussel · BECleveland Clinic Lerner College of Medicine · USUniversity of Queensland · AU

Funding

Molecular Basis of Ang II Receptor FunctionsR01HL057470 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 1997 to 2013
$4.4M
Structure-Guided Studied of GPCRs of RASR01HL132351 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 2017 to 2019
$1.6M
Phosphoproteome and Ang II-induced VSMC Gene ExpressionR01HL083243 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 2006 to 2010
$1.6M
Regulation of AT1R-signaling and pathology in vessels through microRNAR01HL115964 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 2012 to 2015
$1.5M
Mechanism of Cell Death in Expressing AT2 ReceptorR01HL064845 · NHLBI · CLEVELAND CLINIC LERNER COL/MED-CWRU · PI KARNIK, SADASHIVA S. · 2002 to 2005
$1.4M
Structure-Guided Analysis of Mechanisms of AT1R FunctionsR56HL132351 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 2016 to 2016
$548k
AT1R-regulated nuclear functions of Gb2R21HL110043 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI KARNIK, SADASHIVA S · 2011 to 2012
$432k
NHLBI NIH HHS HL115964NHLBI NIH HHS R01 HL057470NHLBI NIH HHS R01 HL064845NHLBI NIH HHS R01 HL083243NHLBI NIH HHS R01 HL115964NHLBI NIH HHS R01 HL132351NHLBI NIH HHS R01 HL57470NHLBI NIH HHS R21 HL110043NHLBI NIH HHS R56 HL132351
6 · The paper itself

Abstract

The renin angiotensin system (RAS) produced hormone peptides regulate many vital body functions. Dysfunctional signaling by receptors for RAS peptides leads to pathologic states. Nearly half of humanity today would likely benefit from modern drugs targeting these receptors. The receptors for RAS peptides consist of three G-protein-coupled receptors—the angiotensin II type 1 receptor (AT1 receptor), the angiotensin II type 2 receptor (AT2 receptor), the MAS receptor—and a type II trans-membrane zinc protein—the candidate angiotensin IV receptor (AngIV binding site). The prorenin receptor is a relatively new contender for consideration, but is not included here because the role of prorenin receptor as an independent endocrine mediator is presently unclear. The full spectrum of biologic characteristics of these receptors is still evolving, but there is evidence establishing unique roles of each receptor in cardiovascular, hemodynamic, neurologic, renal, and endothelial functions, as well as in cell proliferation, survival, matrix-cell interaction, and inflammation. Therapeutic agents targeted to these receptors are either in active use in clinical intervention of major common diseases or under evaluation for repurposing in many other disorders. Broad-spectrum influence these receptors produce in complex pathophysiological context in our body highlights their role as precise interpreters of distinctive angiotensinergic peptide cues. This review article summarizes findings published in the last 15 years on the structure, pharmacology, signaling, physiology, and disease states related to angiotensin receptors. We also discuss the challenges the pharmacologist presently faces in formally accepting newer members as established angiotensin receptors and emphasize necessary future developments.

Indexed as

AnimalsCardiovascular DiseasesCell ProliferationEndotheliumGTP-Binding ProteinsHumansInflammationKidney DiseasesMiceNervous System DiseasesPolymorphism, GeneticProtein-Tyrosine KinasesReactive Oxygen SpeciesReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Receptor Protein-Tyrosine KinasesAT4 receptorGTP-Binding ProteinsProtein-Tyrosine KinasesReactive Oxygen SpeciesReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Receptor Protein-Tyrosine KinasesReceptors, Angiotensin

Identifiers

PMID26315714
PMCPMC4630565
OpenAlexW2116084547

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.