Saved in:
| Main Author: | |
|---|---|
| Format: | Recurso digital |
| Language: | |
| Published: |
Zenodo
2025
|
| Online Access: | https://doi.org/10.5281/zenodo.15447055 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Table of Contents:
- <p> </p> <p>Abstract: Doxorubicin (DOX), a cornerstone of numerous cancer chemotherapy regimens, is unfortunately associated with a significant and often irreversible cardiotoxicity, termed doxorubicin-induced cardiotoxicity (DIC). This debilitating side effect can manifest acutely, in the early stages of treatment, or years after its completion, leading to heart failure and a diminished quality of life for cancer survivors. The pathogenesis of DIC is multifactorial, involving oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis of cardiomyocytes. However, emerging evidence increasingly highlights the critical role of the gut microbiota – the complex community of microorganisms residing in the gastrointestinal tract – as a significant modulator of systemic health and disease, including cardiovascular function.</p> <p>This comprehensive review posits that the gut microbiota profoundly influences the development and severity of DIC through intricate bidirectional communication pathways, collectively known as the gut-heart axis. We explore the impact of DOX on the delicate balance of the gut microbial ecosystem, leading to dysbiosis characterized by alterations in microbial diversity, composition, and metabolic function. This drug-induced dysbiosis can compromise the integrity of the intestinal barrier, facilitating the translocation of pro-inflammatory microbial products into the systemic circulation. These microbial components, along with altered levels of microbial metabolites such as short-chain fatty acids (SCFAs) and trimethylamine-N-oxide (TMAO), can trigger and exacerbate systemic inflammation, a key driver of DIC. Furthermore, the gut microbiota can modulate oxidative stress pathways, directly and indirectly impacting cardiomyocyte health.</p>