A mechanistic computational model of the HIF signaling pathway in endothelial cells.

Rebeca Hannah de Melo Oliveira, Arvind P Pathak, Aleksander S Popel

Abstract read

In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

–field-weighted citation impact

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

1 citing paper in PubMed.

Dynamic functional connectivity variability may explain hypoxia-induced cognitive impairment at high-altitude.iScience · 2026
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.

Rebeca Hannah de Melo OliveiraDepartment of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Arvind P PathakDepartment of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Aleksander S PopelDepartment of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In conditions such as cancer, cardiovascular diseases, and retinal diseases, cells under hypoxia activate oxygen-sensing mechanisms, promoting adaptation and survival. Many hypoxia computational models predate standardized identifiability analyses and lack systematic treatment of the HIF isoform-specific dynamics in endothelial cells. We present a technically validated mechanistic model of the HIF pathway in endothelial cells, capturing graded oxygen sensitivity and the transition from HIF1α-dominated acute to HIF2α-dominated prolonged hypoxic responses. Following identifiability analyses, the model was calibrated and validated against independent datasets, achieving Pearson correlations of 0.7-0.95 and no systematic residual bias (Runs test

Indexed as

Computational bioinformaticsMolecular biologySystems biology

Identifiers

PMID42291256

DOI10.1016/j.isci.2026.116195

PMCPMC13253090

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.