AI Article Synopsis
- Doxorubicin (DOX) is an effective chemotherapy drug for treating various cancers but can cause significant organ damage, particularly to the heart.
- The study focused on the effects of DOX on autophagy in two types of mouse fibroblasts: mouse embryonic fibroblasts (NIH3T3) and primary cardiac fibroblasts.
- Results showed that DOX increased autophagy markers in NIH3T3 cells while not affecting cardiac fibroblasts, indicating that DOX influences autophagy differently depending on the cell type.
Article Abstract
Doxorubicin (DOX) is a highly effective chemotherapeutic used to treat many adult and pediatric cancers, such as solid tumors, leukemia, lymphomas and breast cancer. It can also cause injuries to multiple organs, including the heart, liver, and brain or kidney, although cardiotoxicity is the most prominent side effect of DOX. In this study, we examined the potential effects of DOX on autophagy activity in two different mouse fibroblasts. Mouse embryonic fibroblasts (NIH3T3) and mouse primary cardiac fibroblasts (CFs) were treated with DOX to assess changes in the expression of two commonly used autophagy protein markers, LC3II and p62. We also examined the effects of DOX the on expression of key genes that encode components of the molecular machinery and regulators modulating autophagy in response to both extracellular and intracellular signals. We observed that LC3II levels increased and p62 levels decreased following the DOX treatment in NIH3T3 cells. However, similar effects were not observed in primary cardiac fibroblasts. In addition, DOX treatment induced the upregulation of a significant number of genes involved in autophagy in NIH3T3 cells, but not in primary cardiac fibroblasts. Taken together, these results indicate that DOX upregulates autophagy in fibroblasts in a cell-specific manner.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11648171 | PMC |
| http://dx.doi.org/10.1177/09603271241231947 | DOI Listing |
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