Levetiracetam elicits sub-chronic cardiotoxicity via modulating TLR4/MyD88 and NF-κB signaling axis: Mechanistic validation across molecular, functional, and structural endpoints

Mohammad Y. Alqahtani

doi:10.1016/j.tice.2026.103564

Levetiracetam elicits sub-chronic cardiotoxicity via modulating TLR4/MyD88 and NF-κB signaling axis: Mechanistic validation across molecular, functional, and structural endpoints

2026-04-30

0

PRE

AI

M

Mohammad Y. Alqahtani

A

Abdullah Alghamdi

S

Suad A. Alghamdi

A

Abdulkarim S. Binshaya

A

Awaji Y. Safhi

F

Fahad Y. Sabei

A

Adil Abalkhail

M

Mohammed Alissa *

DOI：10.1016/j.tice.2026.103564

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Abstract

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• Levetiracetam dysregulated TLR4/MyD88 and NF-κB pathway • Levetiracetam provoked myocardial toxicity via promoting oxidative stress • Severe echocardiographic alterations were found after Levetiracetam exposure • Levetiracetam disrupted cardiac function markers and apoptotic indices • Levetiracetam instigated histopathological damages in cardiac tissues

Keywords:

Levetiracetam

cardiotoxicity

TLR4/MyD88

NF-κB

oxidative stress

Levetiracetam elicits sub-chronic cardiotoxicity via modulating TLR4/MyD88 and NF-κB signaling axis: Mechanistic validation across molecular, functional, and structural endpoints

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