Evidence map›Paper›PMID 34680115›Full record

ReviewBiomolecules2021

Biomolecules Orchestrating Cardiovascular Calcification.

Yin Tintut, Henry M Honda, Linda L Demer

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Collagen VIII in vascular diseases.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Review
  5. Invasive electrochemical impedance spectroscopy with phase delay for experimental atherosclerosis phenotyping.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Article
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

3 authors at 1 institution in 1 country.

Yin TintutDepartment of Medicine, University of California-Los Angeles, Los Angeles, CA 90095, USA.
Henry M HondaDepartment of Medicine, University of California-Los Angeles, Los Angeles, CA 90095, USA.
Linda L DemerDepartment of Medicine, University of California-Los Angeles, Los Angeles, CA 90095, USA.
University of California, Los Angeles · US

Funding

Role of intermittent activation of parathyroid hormone receptor in exercise-induced vascular calcificationR01HL151391 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2021 to 2024
$2.2M
Serotonin receptor contribution to inflammation-induced calcific aortic valve diseaseR01HL137647 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2019 to 2022
$1.6M
Does aging transform calcific vasculopathy into a plaque stabilizing process?R21AG061586 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2019 to 2020
$429k
NHLBI NIH HHS R01 HL137647NHLBI NIH HHS R01 HL151391NIA NIH HHS R21 AG061586
6 · The paper itself

Abstract

Vascular calcification, once considered a degenerative, end-stage, and inevitable condition, is now recognized as a complex process regulated in a manner similar to skeletal bone at the molecular and cellular levels. Since the initial discovery of bone morphogenetic protein in calcified human atherosclerotic lesions, decades of research have now led to the recognition that the regulatory mechanisms and the biomolecules that control cardiovascular calcification overlap with those controlling skeletal mineralization. In this review, we focus on key biomolecules driving the ectopic calcification in the circulation and their regulation by metabolic, hormonal, and inflammatory stimuli. Although calcium deposits in the vessel wall introduce rupture stress at their edges facing applied tensile stress, they simultaneously reduce rupture stress at the orthogonal edges, leaving the net risk of plaque rupture and consequent cardiac events depending on local material strength. A clinically important consequence of the shared mechanisms between the vascular and bone tissues is that therapeutic agents designed to inhibit vascular calcification may adversely affect skeletal mineralization and vice versa. Thus, it is essential to consider both systems when developing therapeutic strategies.

Indexed as

AnimalsBiopolymersCalcinosisCalciumCardiovascular DiseasesHumansModels, BiologicalMolecular Targeted TherapyBiopolymersCalciumcalcificationcardiovascularinflammationlipidsskeletal

Identifiers

PMID34680115
PMCPMC8533507
OpenAlexW3206095016

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.