Advances in mitochondrial dysfunction in radiation tissue injury.

Area of Science:

• Oncology
• Radiation Biology
• Cellular Biology

Background:

• Cancer radiotherapy often causes collateral damage to healthy tissues.
• The nucleus was traditionally viewed as the primary radiation target, but mitochondria's role is increasingly recognized.

Purpose of the Study:

• To review mitochondrial dysfunction in various tissues after irradiation.
• To elucidate the mechanisms of radiation-induced mitochondrial damage.
• To summarize key signaling pathways involved in mitochondrial response to radiation.

Main Methods:

• Comprehensive literature review of studies on radiation effects on mitochondria.
• Analysis of mitochondrial alterations in irradiated tissues (intestine, heart, lung, brain, skin, hematopoietic system).
• Summary of signaling pathways regulating mitochondrial response.

Main Results:

• Mitochondrial dysfunction, including altered dynamics, impaired metabolism, increased reactive oxygen species (ROS), and apoptosis/senescence, is central to radiation pathology.
• Key pathways like AMPK/PGC-1α, Nrf2/ARE/TFAM, and NLRP3 inflammasome are involved in mitochondrial response to radiation stress.

Conclusions:

• Mitochondria are critical mediators of radiation-induced tissue injury.
• Targeting mitochondrial pathways presents promising avenues for radioprotection and novel therapeutic strategies in oncology.