Evidence map›Paper›PMID 42539088›Full record

ArticleResearch square2026

Poly-Pharmacologic Disruption of the Proliferative-to-Mesenchymal Fate Branch Point Reverses EndMT and Pulmonary Hypertension.

Dinesh Bharti, Tetiana Kolodiazhna, Sedat Kacar, Mathews V Varghese, Takanori Sano, Sruthi Radhakrishnan, Joel James, A J Hinkle, Maki Niihori, Olga Rafikova and 2 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Dinesh BhartiDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
Tetiana KolodiazhnaDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, 77204-5039.
Sedat KacarDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
Mathews V VargheseDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
Takanori SanoDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
Sruthi RadhakrishnanDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
Joel JamesDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
A J HinkleDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
Maki NiihoriDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
Olga RafikovaDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.
Alexander V StatsyukDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, 77204-5039.
Ruslan RafikovDepartment of Medicine, Division of Pulmonary, Critical Care, Sleep & Occupational Medicine, Indiana University, Indianapolis, Indiana 46202.ORCID 0000-0001-5950-4076

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial-to-mesenchymal transition (EndMT) drives the vascular remodeling in pulmonary arterial hypertension (PAH), yet the regulators that commit endothelial cells to this fate and whether they are pharmacologically addressable remain poorly defined. We report TK22, a small molecule that selectively erases the EndMT-competent endothelial state and reverses experimental pulmonary hypertension. TK22 was developed by structure-based design as an ATP-competitive CDK5 inhibitor (IC

Indexed as

endothelial-to-mesenchymal transitionfate branch pointkinome profilingpolypharmacologypulmonary arterial hypertensionsingle-cell RNA sequencingvascular remodeling

Identifiers

PMID42539088
PMCPMC13419571

What Socratic 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 Socratic graph.