PTX3 from vascular endothelial cells contributes to trastuzumab-induced cardiac complications.
Zhifei XuZizheng GaoHuangxi FuYan ZengYing JinBo XuYuanteng ZhangZezheng PanXueqin ChenXiaochen ZhangXiaohong WangHao YanXiaochun YangBo YangQiaojun HePeihua LuoPublished in: Cardiovascular research (2023)
We identified PTX3 as a potential biomarker and target for the treatment of trastuzumab-induced cardiac complications and demonstrated that lapatinib can prevent cardiac dysfunction caused by trastuzumab by blocking EFGR/STAT3-mediated PTX3 release from VECs, which provided a mechanistic rationale for the combined application of lapatinib and trastuzumab in cancer.
Keyphrases
- metastatic breast cancer
- high glucose
- epidermal growth factor receptor
- endothelial cells
- left ventricular
- diabetic rats
- risk factors
- oxidative stress
- tyrosine kinase
- cell proliferation
- clinical trial
- positive breast cancer
- papillary thyroid
- squamous cell carcinoma
- heart failure
- atrial fibrillation
- combination therapy