Evidence map›Paper›PMID 41448375›Full record

ReviewSeminars in cancer biology2026

Heartbreakers and healers: RNA rebels in cardio-oncology.

Celestina Agyemang-Dua, Charles S Chung, Cristina Espinosa-Diez

Abstract readReview
In one paragraph

Review in Seminars in cancer biology, 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

3 authors.

Celestina Agyemang-DuaCenter for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48202, USA.
Charles S ChungDepartment of Physiology, Wayne State University, Detroit, MI 48202, USA.
Cristina Espinosa-DiezCenter for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48202, USA; Department of Physiology, Wayne State University, Detroit, MI 48202, USA. Electronic address: cristina.espinosa.diez@wayne.edu.

Funding

Leveraging Mechanical Control of Relaxation to Improve Diastolic FunctionR01HL151738 · NHLBI · WAYNE STATE UNIVERSITY · PI CHUNG, CHARLES S · 2021 to 2025
$1.9M
NHLBI NIH HHS R01 HL151738
6 · The paper itself

Abstract

Cancer therapies save lives but often "break hearts" by damaging the cardiovascular system. As survival improves, therapy-induced cardiotoxicity has become a defining challenge of modern oncology. Recent discoveries reveal that long non-coding RNAs (lncRNAs), once dismissed as genomic noise, are the "RNA rebels" orchestrating cellular responses to cancer treatments. These molecules act as both heartbreakers and healers, amplifying or counteracting oxidative stress, mitochondrial dysfunction, apoptosis, and vascular injury. In anthracycline, radiation, and VEGF-targeted therapies, lncRNAs govern key processes that dictate whether cells succumb to damage or mount protective repair responses. Pro-injury lncRNAs exacerbate senescence and inflammation, while protective ones preserve mitochondrial homeostasis and limit cell death. Beyond mechanistic insight, these molecules hold clinical promise as biomarkers and therapeutic targets, guiding RNA-based strategies to predict, prevent, and treat cardiotoxicity. Understanding how they blur the line between protection and harm may redefine how we safeguard the heart in the era of precision cardio oncology.

Indexed as

Antineoplastic AgentsCardiotoxicityNeoplasmsRNA, Long NoncodingAnimalsCardio-OncologyHumansMedical OncologyAntineoplastic AgentsRNA, Long NoncodingCancer TherapyCardiotoxicityLncRNAs

Identifiers

PMID41448375
PMCPMC12861466

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.