Evidence map›Paper›PMID 27974299›Full record

ReviewAmerican journal of physiology. Cell physiology2017

Nitric oxide: what's new to NO?

Kedar Ghimire, Helene M Altmann, Adam C Straub, Jeffrey S Isenberg

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
8.0field-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

100 citing papers in PubMed, 233 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. METTL3 mediates mJournal of advanced research · 2026
    Article
  7. Article
  8. Oxidative Stress and Its Role in Vascular Damage and Atherosclerosis.International journal of molecular sciences · 2026
    Review
  9. Article
  10. Evaluation of Cardiovascular Effects of the Hydroalcoholic Fruit Extract ofCardiovascular & hematological disorders drug targets · 2026
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Palmitoylation in cardiovascular diseases: Molecular mechanism and therapeutic potential.International journal of cardiology. Heart & vasculature · 2025
    Review
  18. Review
  19. Review
  20. Review

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

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

4 authors at 1 institution in 1 country.

Kedar GhimireHeart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania.
Helene M AltmannHeart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania.
Adam C StraubHeart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania.
Jeffrey S IsenbergHeart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania; jsi5@pitt.edu.
University of Pittsburgh · US

Funding

TRAINING PROGRAM FOR MD/PHD STUDENTST32GM008208 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STEINMAN, RICHARD A · 1987 to 2021
$15.4M
Vascular Smooth Muscle and Blood Pressure Regulation By Cyb5R3²R01HL128304 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STRAUB, ADAM CARL · 2016 to 2020
$2.4M
Bioengineering Tracheas Through Targeting Activated CD47R21EB017184 · NIBIB · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BADYLAK, STEPHEN F. · 2014 to 2015
$423k
NHLBI NIH HHS R01 HL128304NIBIB NIH HHS R21 EB017184NIGMS NIH HHS T32 GM008208
6 · The paper itself

Abstract

Nitric oxide (NO) is one of the critical components of the vasculature, regulating key signaling pathways in health. In macrovessels, NO functions to suppress cell inflammation as well as adhesion. In this way, it inhibits thrombosis and promotes blood flow. It also functions to limit vessel constriction and vessel wall remodeling. In microvessels and particularly capillaries, NO, along with growth factors, is important in promoting new vessel formation, a process termed angiogenesis. With age and cardiovascular disease, animal and human studies confirm that NO is dysregulated at multiple levels including decreased production, decreased tissue half-life, and decreased potency. NO has also been implicated in diseases that are related to neurotransmission and cancer although it is likely that these processes involve NO at higher concentrations and from nonvascular cell sources. Conversely, NO and drugs that directly or indirectly increase NO signaling have found clinical applications in both age-related diseases and in younger individuals. This focused review considers recently reported advances being made in the field of NO signaling regulation at several levels including enzymatic production, receptor function, interacting partners, localization of signaling, matrix-cellular and cell-to-cell cross talk, as well as the possible impact these newly described mechanisms have on health and disease.

Indexed as

Models, CardiovascularAnimalsBlood Flow VelocityBlood VesselsCardiovascular DiseasesHumansNeovascularization, PhysiologicNitric OxideNitric OxidecardiaccardiovascularCD47cytochrome b5 reductase 3matricellularnitric oxideNOSsignal transductionthrombospondin-1

Identifiers

PMID27974299
PMCPMC5401944
OpenAlexW2565159046

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.