Key result
ER stress disrupts gut integrity to drive inflammation-mediated antineoplastic cardiovascular toxicity.
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This review highlights the mechanistic role of endoplasmic reticulum stress in gut barrier disruption and suggests it as a potential therapeutic target for antineoplastic drug-related cardiovascular toxicity.
Endoplasmic reticulum (ER) stress is extensively studied as a pivotal role in the pathological processes associated with intestinal microecology. In antineoplastic drug treatments, ER stress is implicated in altering the permeability of the mechanical barrier, depleting the chemical barrier, causing dysbiosis, exacerbating immune responses and inflammation in the immune barrier. Enteric dysbiosis and intestinal dysfunction significantly affect the circulatory system in various heart disorders. In antineoplastic drug-related cardiovascular (CV) toxicity, ER stress constitutes a web of relationships in the host-microbiome symbiotic regulatory loop. Therefore, understanding the holobiont perspective will help de-escalate spatial and temporal restrictions. This review investigates the role of ER stress-mediated gut microecological alterations in antineoplastic treatment-induced CV toxicity. • Gut barrier-driven inflammation accounts for cardiovascular toxicity of cancer drugs. • Endoplasmic reticulum stress disrupts gut integrity through interconnected pathways. • Targeting endoplasmic reticulum stress and gut barriers may alleviate cardiotoxicity.
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Zhang et al. (2024) conducted a review in Antineoplastic drug-related cardiovascular toxicity. Endoplasmic reticulum stress and gut microecological alterations was evaluated. Endoplasmic reticulum stress disrupts gut integrity and mediates gut barrier-driven inflammation, which contributes to antineoplastic drug-related cardiovascular toxicity.
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