| Literature DB >> 31022376 |
Raghu P Kataru1, Itay Wiser1, Jung Eun Baik1, Hyeung Ju Park1, Sonia Rehal1, Jin Yeon Shin1, Babak J Mehrara2.
Abstract
Secondary lymphedema is a common complication of cancer treatment resulting in progressive fibroadipose tissue deposition, increased risk of infections, and, in rare cases, secondary malignancies. Until recently, the pathophysiology of secondary lymphedema was thought to be related to impaired collateral lymphatic formation after surgical injury. However, more recent studies have shown that chronic inflammation-induced fibrosis plays a key role in the pathophysiology of this disease. In this review, we will discuss the evidence supporting this hypothesis and summarize recent publications demonstrating that lymphatic injury activates chronic immune responses that promote fibrosis and lymphatic leakiness, decrease collecting lymphatic pumping, and impair collateral lymphatic formation. We will review how chronic mixed T-helper cell inflammatory reactions regulate this process and how this response may be used to design novel therapies for lymphedema.Entities:
Mesh:
Year: 2019 PMID: 31022376 DOI: 10.1016/j.trsl.2019.04.001
Source DB: PubMed Journal: Transl Res ISSN: 1878-1810 Impact factor: 7.012