TY - JOUR
AR - COCB-2019-1-102
TI - The Pathway from Radiation to Fibrosis: LET Dependence
AU - Huichen, Wang
AU - Kareena M., Menezes
AU - Premkumar B., Saganti
JO - Clinical Oncology and Cancer Biology
PY - 2019
DA - Mon 16, Dec 2019
SN - 2733-2276
DO - http://dx.doi.org/10.31487/j.COCB.2019.01.02
UR - https://www.sciencerepository.org/the-pathway-from-radiation-to-fibrosis_COCB-2019-1-102 
KW - Radiation-induced fibrosis (RIF), myofibroblasts, reactive oxygen species (ROS), transforming growth factor-β (TGF-β), linear energy transfer (LET)
AB - 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.