What is the clinical evidence from this study?

Population: Doxorubicin-induced endothelial dysfunction. Intervention: Doxorubicin vs. Control (saline). Primary outcome: Endothelial monolayer permeability (Cohen’s d 1.0, p=<0.05).

What question did this study set out to answer?

To explore the lasting effects of doxorubicin on endothelial cells after chemotherapy completion.

January 9, 2026Cardio-OncologyOpen Access

Sustained mesenchymal reprogramming of endothelial cells after completion of chemotherapy

Q: What are the key findings of this study?

Doxorubicin treatment leads to sustained mesenchymal reprogramming and compromised endothelial barrier function post-treatment.

Q: What does this research mean for the field?

Doxorubicin treatment leads to sustained mesenchymal reprogramming and compromised endothelial barrier function post-treatment. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To explore the lasting effects of doxorubicin on endothelial cells after chemotherapy completion.

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Key result

Doxorubicin treatment leads to sustained mesenchymal reprogramming and compromised endothelial barrier function post-treatment.

Key Points

To explore the lasting effects of doxorubicin on endothelial cells after chemotherapy completion.
Used a doxorubicin treatment/washout model to assess endothelial cell changes.
Conducted ChIP sequencing and transcriptomic analysis to evaluate gene expression.
Implemented a selective ALK4/5/7 receptor kinase inhibitor (SB431542) to investigate TGF-β/activin pathway roles.
Analyzed cytoskeletal changes and permeability in treated endothelial cells.
Doxorubicin washout triggered sustained mesenchymal reprogramming in endothelial cells.
Upregulation of fibroblastic and smooth muscle lineage transcripts was observed.
SB431542 treatment inhibited mesenchymal marker expression and cytoskeletal rearrangements.
Increased endothelial monolayer permeability was reversed with SB treatment.

PICO

Population

Doxorubicin-induced endothelial dysfunction

Intervention / Comparator

Doxorubicin vs Control (saline) (5 mg/kg)

Primary Outcome

Endothelial monolayer permeability — Cohen’s d 1.0, p=<0.05

Main Result

Effect estimate: Cohen’s d 1.0

p-value: p=<0.05

Limitations

Lack of specific patient demographic data
Limited sample size for certain analysis

Discussion

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Implication

Uncovers the mechanism of endothelial cell reprogramming after doxorubicin treatment, highlighting cardiac risk.

Cite This Study

Sjostrom et al. (2025) studied Doxorubicin-induced endothelial dysfunction. Doxorubicin vs. Control (saline) was evaluated on Endothelial monolayer permeability (Cohen’s d 1.0, p=<0.05). Doxorubicin treatment leads to sustained mesenchymal reprogramming and compromised endothelial barrier function post-treatment.

synapsesocial.com/papers/696128f244c2cd6c68456c7d https://doi.org/10.1186/s40959-025-00413-7

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Sustained mesenchymal reprogramming of endothelial cells after completion of chemotherapy

Key Points

PICO

Main Result

Limitations

Discussion

Implication

Cite This Study

Sustained mesenchymal reprogramming of endothelial cells after completion of chemotherapy

Key Points

PICO

Main Result

Limitations

Discussion

Implication

Cite This Study

Also Consider

Also Consider