Student or educator? Sign up with your school email and get 6 months of Pro free.
Cited by 653

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Molecular pathogenesis of pulmonary arterial hypertension

Open access
Rabinovitch, Marlene·2012·Journal of Clinical Investigation

Abstract

Recent clinical and experimental studies are redefining the cellular and molecular bases of pulmonary arterial hypertension (PAH).The genetic abnormalities first identified in association with the idiopathic form of PAH -together with a vast increase in our understanding of cell signaling, cell transformation, and cell-cell interactions; gene expression; microRNA processing; and mitochondrial and ion channel function -have helped explain the abnormal response of vascular cells to injury.Experimental and clinical studies now converge on the intersection and interactions between a genetic predisposition involving the BMPR2 signaling pathway and an impaired metabolic and chronic inflammatory state in the vessel wall.These deranged processes culminate in an exuberant proliferative response that occludes the pulmonary arterial (PA) lumen and obliterates the most distal intraacinar vessels.Here, we describe emerging therapies based on preclinical studies that address these converging pathways.

Overview

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.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1172/jci60658

Cites

4 of 4 references verified0 citation errors · 0 not checkable

Statistics

Verification

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.

A few free checks a day · papers already verified open instantly · results are public

Self-check

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

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

Citations

Cites

Show all 4 references

Cited by

See all 653

Metadata

Authors
Rabinovitch, M.
Venue
Journal of Clinical Investigation
Published
2012-12-03
Volume
122
Issue
12
Pages
4306-4313
ISSN
0021-9738 (ISSN-L)
OpenAlex
W4293257851
Cited by
653
References
4
FWCI
32.96
Type
journal article
Language
en
Open access
bronze

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

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Molecular pathogenesis of pulmonary arterial hypertension. https://app.cochat.ai/papers/10.1172/jci60658
The paper
Rabinovitch, M. (2012). Molecular pathogenesis of pulmonary arterial hypertension. Journal of Clinical Investigation. https://doi.org/10.1172/jci60658

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.