Evidence map›Paper›PMID 27233763›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2016

Intracrine angiotensin II functions originate from noncanonical pathways in the human heart.

Carlos M Ferrario, Sarfaraz Ahmad, Jasmina Varagic, Che Ping Cheng, Leanne Groban, Hao Wang, James F Collawn, Louis J Dell Italia

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

37 citing papers in PubMed, 61 citations in OpenAlex.

  1. Fibroblasts under pressure: cardiac fibroblast responses to hypertension and antihypertensive therapies.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  2. Article
  3. Heart Failure in Menopause: Treatment and New Approaches.International journal of molecular sciences · 2022
    Review
  4. Article
  5. Review
  6. Review
  7. Antisense Inhibition of Angiotensinogen With IONIS-AGT-LJACC. Basic to translational science · 2021
    Article
  8. Article
  9. Review
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  13. Article
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  17. Article
  18. Should ACE inhibitors and ARBs be used in combination in children?Pediatric nephrology (Berlin, Germany) · 2019
    Article
  19. Article
  20. The renin-angiotensin-aldosterone system and its suppression.Journal of veterinary internal medicine · 2019
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Carlos M FerrarioDepartments of Surgery, Internal Medicine-Nephrology and Physiology-Pharmacology, Wake Forest University Health Science Center, Winston-Salem, North Carolina; cferrari@wakehealth.edu.
Sarfaraz AhmadDepartments of Surgery, Internal Medicine-Nephrology and Physiology-Pharmacology, Wake Forest University Health Science Center, Winston-Salem, North Carolina;
Jasmina VaragicDepartments of Surgery, Internal Medicine-Nephrology and Physiology-Pharmacology, Wake Forest University Health Science Center, Winston-Salem, North Carolina; Hypertension and Vascular Research Center, Wake Forest University Health Science Center, Winston-Salem, North Carolina;
Che Ping ChengSection on Cardiovascular Medicine, Department of Internal Medicine, Wake Forest University Health Science Center, Winston-Salem, North Carolina;
Leanne GrobanHypertension and Vascular Research Center, Wake Forest University Health Science Center, Winston-Salem, North Carolina; Department of Anesthesiology, Wake Forest University Health Science Center, Winston-Salem, North Carolina;
Hao WangDepartment of Anesthesiology, Wake Forest University Health Science Center, Winston-Salem, North Carolina;
James F CollawnDepartments of Cell Biology, Microbiology, Physiology, University of Alabama Birmingham, Alabama; and.
Louis J Dell ItaliaDepartments of Cell Biology, Microbiology, Physiology, University of Alabama Birmingham, Alabama; and Division of Cardiovascular Disease, University of Alabama at Birmingham and Department of Veterans Affairs, Birmingham Veterans Affairs Medical Center, Birmingham, Alabama.
Wake Forest University · USBirmingham VA Medical Center · USUniversity of Alabama at Birmingham · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DELL'ITALIA, LOUIS J. · 1994 to 2019
$34.8M
New Molecular Target for Cardiac AgingR01AG049770 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHENG, HENG-JIE · 2015 to 2019
$1.6M
Beta3-Adrenergic Receptor &Progression to Heart FailureR01HL074318 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHENG, CHE-PING · 2003 to 2006
$1.3M
NHLBI NIH HHS P01 HL051952NHLBI NIH HHS R01 HL074318NIA NIH HHS R01 AG049770
6 · The paper itself

Abstract

Although it is well-known that excess renin angiotensin system (RAS) activity contributes to the pathophysiology of cardiac and vascular disease, tissue-based expression of RAS genes has given rise to the possibility that intracellularly produced angiotensin II (Ang II) may be a critical contributor to disease processes. An extended form of angiotensin I (Ang I), the dodecapeptide angiotensin-(1-12) [Ang-(1-12)], that generates Ang II directly from chymase, particularly in the human heart, reinforces the possibility that an alternative noncanonical renin independent pathway for Ang II formation may be important in explaining the mechanisms by which the hormone contributes to adverse cardiac and vascular remodeling. This review summarizes the work that has been done in evaluating the functional significance of Ang-(1-12) and how this substrate generated from angiotensinogen by a yet to be identified enzyme enhances knowledge about Ang II pathological actions.

Indexed as

Renin-Angiotensin SystemAngiotensin IIAngiotensinogenAnimalsChymasesHeartHumansMyocardiumPeptide FragmentsVascular RemodelingVentricular Remodelingangiotensin-(1-12), humanAngiotensin IIAngiotensinogenChymasesPeptide Fragmentsangiotensin-(1–12), angiotensin converting enzyme inhibitorsheart chymaseheart failurehypertension

Identifiers

PMID27233763
PMCPMC5008653
OpenAlexW2401791153

What OpenQuestion 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 OpenQuestion graph.