The Pathway from Radiation to Fibrosis: LET Dependence

Author Info

Huichen Wang Kareena M. Menezes Premkumar B. Saganti

Corresponding Author

Premkumar B. Saganti
Texas A&M Chancellor's Research Initiative, Radiation Institute for Science and Engineering, Prairie View A&M University, Texas, United States

A B S T R A C T

It is well-known that Radiation-induced fibrosis (RIF) is a late event occurring months to years after the initial radiation exposure. Fibrotic lesions have been shown to manifest in many tissues including the skin, heart, lung, liver and kidney. Fibrosis occurs due to abnormal accumulation of extracellular matrix (ECM) proteins that result in loss of normal tissue and organ function. The cell type involved in RIF is myofibroblasts, which do not undergo apoptosis after healing but instead continue to accumulate, producing excessive amounts of ECM proteins, thereby damaging the tissues and organs. Reactive oxygen species, generated in response to radiation, is one signal that helps maintain the myofibroblast phenotype. In this review, we discuss molecular mechanisms leading to this late radiation event, known biomarkers for prediction, preclinical animal models of radiation-induced toxicity and current clinical trials designed for mitigation and treatment of radiation-induced fibrosis. We also discuss other physical properties such as linear energy transfer (LET) than the ones used in the clinics today which may have the potential to change our understanding on this inevitable pathway from radiation treatment to organ fibrosis.

Article Info

Article Type

Review Article

Publication history

Received: Wed 27, Nov 2019
Accepted: Fri 06, Dec 2019
Published: Mon 16, Dec 2019

Copyright

© 2023 Premkumar B. Saganti. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.
DOI: 10.31487/j.COCB.2019.01.02