B-Fe3O4NPs did not induce cell apoptosis or necrosis in HUVECs within 24 h.
B-Fe3O4NPs induced HUVEC dysfunction and inflammation.
B-Fe3O4NPs induced enhanced autophagic activity and blockade of autophagy flux.
Suppression of autophagy dysfunction attenuated B-Fe3O4NP-induced HUVEC dysfunction.