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Aims/Introduction  Cell death‐inducing  DFF 45‐like effector C ( CIDEC ) was proven to be closely associated with the development of insulin resistance and metabolic syndrome. We aimed to investigate whether   CIDEC   gene silencing could alleviate pulmonary vascular remodeling in a type 2 diabetes rat model.    Materials and Methods  We built a type 2 diabetes rat model. An adenovirus harboring  CIDEC  small interfering ribonucleic acid was then injected into the jugular vein to silence the   CIDEC   gene. After hematoxylin–eosin and Sirius red staining, we detected indexes of the pulmonary arterioles remodeling. Immunohistochemical staining of proliferating cell nuclear antigen was used to evaluate the pulmonary arterial smooth muscle cell proliferation. Apoptosis was evaluated by terminal deoxynucleotidyl transferase  dUTP  nick end labeling reaction and western blotting. The levels of signaling pathway proteins expression were measured by western blotting analyses.    Results  Histological analysis of the pulmonary artery showed that the thickness of the adventitia and medial layer increased notably in type 2 diabetes rats. Immunohistochemistry showed that more proliferating cell nuclear antigen‐positive pulmonary arterial smooth muscle cells could be seen in type 2 diabetes rats; and after   CIDEC   gene silencing, proliferating cell nuclear antigen positive cells decreased accordingly. Cleaved caspase‐3 and cleaved poly (adenosine diphosphate‐ribose) polymerase measured by western blotting showed increased apoptosis with overexpressed  CIDEC  in diabetes. Terminal deoxynucleotidyl transferase  dUTP  nick end labeling reaction showed that the apoptosis mainly occurred in endothelial cells. Western blotting analysis showed  CIDEC  overexpression in rats with diabetes, and phosphorylated adenosine 5′ monophosphate‐activated protein kinase‐α expression was significantly decreased. After   CIDEC   gene silencing, the expression of phosphorylated adenosine 5′ monophosphate‐activated protein kinase‐α was upregulated.    Conclusions  The  CIDEC /5′ monophosphate‐activated protein kinase signaling pathway could be a potential therapeutic candidate against pulmonary vascular diseases in type 2 diabetes patients.

Cell death‐inducing DFF 45‐like effector C gene silencing alleviates pulmonary vascular remodeling in a type 2 diabetic rat model