Reply to Trela, B.A.; Guffroy, M.R. Comment on “AlAsmari et al. Venetoclax Induces Cardiotoxicity Through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway. Int. J. Mol. Sci. 2022, 23, 6260”

Q: What is the clinical evidence from this study?

Study design: Letter. Population: Cardiotoxicity. Intervention: Venetoclax vs. Control.

Q: What does this research mean for the field?

Venetoclax induces cardiotoxicity by modulating oxidative-stress-mediated cardiac inflammation and apoptosis via the NF-κB and BCL-2 pathways. Novelty: ClaimNovelty.CONFIRMATORY. Consensus alignment: ConsensusAlignment.NEUTRAL.

Abdullah F. Alasmari; Adel Alghamdi; Nemat Ali; Fawaz Alasmari

doi:10.3390/ijms27146166

July 10, 2026International Journal of Molecular SciencesOpen Access

Reply to Trela, B.A.; Guffroy, M.R. Comment on “AlAsmari et al. Venetoclax Induces Cardiotoxicity Through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway. Int. J. Mol. Sci. 2022, 23, 6260”

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Key result

The authors clarified their methodology regarding venetoclax-induced cardiotoxicity in an animal model, defending their use of histopathology scoring and cardiac biomarkers like CK-MB and troponin.

Why the study?

Does venetoclax induce cardiotoxicity in a preclinical rat model?

Key Points

Address concerns raised in a letter to the editor regarding the methodology, cardiac biomarker selection, and mechanistic evidence for venetoclax-induced cardiotoxicity via BCL-2 pathway modulation.
Reviewed clinical adverse event reports and pharmacovigilance data regarding cardiotoxicity in patients treated with venetoclax regimens.
Clarified experimental protocols, including the formulation of venetoclax (99.5% purity in 5% DMSO and 0.9% NaCl), blinded histopathological grading of myocardial injury across ten fields per heart section in three animals, and cardiomyocyte cross-sectional area measurements using ImageJ.
Cited clinical evidence showing 34 out of 170 AML patients (20%) treated with venetoclax plus hypomethylating agents experienced 48 cardiac adverse events, most commonly decreased left ventricular ejection fraction (10 patients [21%]) and elevated troponin (7 patients [15%]).
Noted database findings associating venetoclax with higher morbidity and mortality from cardiac adverse events (29.4%) compared to ibrutinib, idelalisib, and acalabrutinib cohorts.
Clarified that while relative heart weight significantly increased in treated animals, absolute heart weight showed a slight non-significant increase, and acknowledged the lack of direct cardiac functional measurements as a study limitation.

Structured PICO

Does venetoclax induce cardiotoxicity in a preclinical rat model?

P

Population

Rats (preclinical model for evaluating cardiotoxicity)

I

Intervention

Venetoclax (VTX) dissolved in 5% DMSO in 0.9% NaCl

C

Comparator

Control group (handled and processed using the same procedures)

O

Outcome

Cardiotoxicity (evaluated via histopathology, cardiac troponin, CK-MB, and inflammatory cytokines)safety

Limitations

Did not measure cardiac function to better evaluate the effect of venetoclax on the heart
Histopathology findings can be spontaneous effects commonly reported in rats rather than treatment-related
Did not measure cardiac function to better evaluate the effect of VTX on the heart

Implication

This reply defends the authors' preclinical findings that venetoclax induces cardiotoxicity through oxidative stress and apoptosis, highlighting the need for further investigation into its cardiac safety profile.

Abstract

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Discussion

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Cite This Study

Alasmari et al. (2026) conducted a letter in Cardiotoxicity. Venetoclax vs. Control was evaluated. The authors clarified their methodology regarding venetoclax-induced cardiotoxicity in an animal model, defending their use of histopathology scoring and cardiac biomarkers like CK-MB and troponin.

synapsesocial.com/papers/6a5331064f7abc118aded7cd https://doi.org/10.3390/ijms27146166

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Reply to Trela, B.A.; Guffroy, M.R. Comment on “AlAsmari et al. Venetoclax Induces Cardiotoxicity Through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway. Int. J. Mol. Sci. 2022, 23, 6260”

Key Points

Structured PICO

Limitations

Implication

Abstract

Discussion

Cite This Study

Reply to Trela, B.A.; Guffroy, M.R. Comment on “AlAsmari et al. Venetoclax Induces Cardiotoxicity Through Modulation of Oxidative-Stress-Mediated Cardiac Inflammation and Apoptosis via NF-κB and BCL-2 Pathway. Int. J. Mol. Sci. 2022, 23, 6260”

Key Points

Structured PICO

Limitations

Implication

Abstract

Discussion

Cite This Study

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