TY - JOUR
T1 - The role of connexin proteins and their channels in radiation‑induced atherosclerosis
AU - Ramadan, Raghda
AU - Baatout, Sarah
AU - Aerts, An
AU - Leybaert, Luc
N1 - Score=10
PY - 2021/1/3
Y1 - 2021/1/3
N2 - Radiotherapy is an effective treatment for breast cancer and other thoracic tumors. However, while high-energy radiotherapy
treatment successfully kills cancer cells, radiation exposure of the heart and large arteries cannot always be avoided, resulting
in secondary cardiovascular disease in cancer survivors. Radiation-induced changes in the cardiac vasculature may thereby
lead to coronary artery atherosclerosis, which is a major cardiovascular complication nowadays in thoracic radiotherapytreated
patients. The underlying biological and molecular mechanisms of radiation-induced atherosclerosis are complex and
still not fully understood, resulting in potentially improper radiation protection. Ionizing radiation (IR) exposure may damage
the vascular endothelium by inducing DNA damage, oxidative stress, premature cellular senescence, cell death and inflammation,
which act to promote the atherosclerotic process. Intercellular communication mediated by connexin (Cx)-based
gap junctions and hemichannels may modulate IR-induced responses and thereby the atherosclerotic process. However, the
role of endothelial Cxs and their channels in atherosclerotic development after IR exposure is still poorly defined. A better
understanding of the underlying biological pathways involved in secondary cardiovascular toxicity after radiotherapy would
facilitate the development of effective strategies that prevent or mitigate these adverse effects. Here,
AB - Radiotherapy is an effective treatment for breast cancer and other thoracic tumors. However, while high-energy radiotherapy
treatment successfully kills cancer cells, radiation exposure of the heart and large arteries cannot always be avoided, resulting
in secondary cardiovascular disease in cancer survivors. Radiation-induced changes in the cardiac vasculature may thereby
lead to coronary artery atherosclerosis, which is a major cardiovascular complication nowadays in thoracic radiotherapytreated
patients. The underlying biological and molecular mechanisms of radiation-induced atherosclerosis are complex and
still not fully understood, resulting in potentially improper radiation protection. Ionizing radiation (IR) exposure may damage
the vascular endothelium by inducing DNA damage, oxidative stress, premature cellular senescence, cell death and inflammation,
which act to promote the atherosclerotic process. Intercellular communication mediated by connexin (Cx)-based
gap junctions and hemichannels may modulate IR-induced responses and thereby the atherosclerotic process. However, the
role of endothelial Cxs and their channels in atherosclerotic development after IR exposure is still poorly defined. A better
understanding of the underlying biological pathways involved in secondary cardiovascular toxicity after radiotherapy would
facilitate the development of effective strategies that prevent or mitigate these adverse effects. Here,
KW - Review article CMLS
KW - Connexin
KW - Intercellular communication
KW - Ionizing radiation
KW - Atherosclerosis
KW - Bystander effect
KW - Gap junction
KW - Hemichannels
UR - https://ecm.sckcen.be/OTCS/llisapi.dll/open/42035777
U2 - 10.1007/s00018-020-03716-3
DO - 10.1007/s00018-020-03716-3
M3 - Article
SN - 1420-682X
VL - 78
SP - 3087
EP - 3103
JO - Cellular and Molecular Life Science
JF - Cellular and Molecular Life Science
ER -