Complex Interplay between DNA Damage and Autophagy in Disease and Therapy.
Aman SinghNaresh RavendranathanJefferson C FrisbeeKrishna K SinghPublished in: Biomolecules (2024)
Cancer, a multifactorial disease characterized by uncontrolled cellular proliferation, remains a global health challenge with significant morbidity and mortality. Genomic and molecular aberrations, coupled with environmental factors, contribute to its heterogeneity and complexity. Chemotherapeutic agents like doxorubicin (Dox) have shown efficacy against various cancers but are hindered by dose-dependent cytotoxicity, particularly on vital organs like the heart and brain. Autophagy, a cellular process involved in self-degradation and recycling, emerges as a promising therapeutic target in cancer therapy and neurodegenerative diseases. Dysregulation of autophagy contributes to cancer progression and drug resistance, while its modulation holds the potential to enhance treatment outcomes and mitigate adverse effects. Additionally, emerging evidence suggests a potential link between autophagy, DNA damage, and caretaker breast cancer genes BRCA1/2, highlighting the interplay between DNA repair mechanisms and cellular homeostasis. This review explores the intricate relationship between cancer, Dox-induced cytotoxicity, autophagy modulation, and the potential implications of autophagy in DNA damage repair pathways, particularly in the context of BRCA1/2 mutations.
Keyphrases
- dna damage
- dna repair
- oxidative stress
- cell death
- endoplasmic reticulum stress
- signaling pathway
- papillary thyroid
- cancer therapy
- diabetic rats
- global health
- squamous cell
- drug delivery
- heart failure
- public health
- gene expression
- stem cells
- dna methylation
- multiple sclerosis
- human health
- lymph node metastasis
- brain injury
- atrial fibrillation
- breast cancer risk
- resting state
- cell therapy
- transcription factor
- functional connectivity
- climate change
- replacement therapy