Both cognitive impairment and cardiovascular diseases have a high incidence in the elderly population, increasing the burden of care and reducing the quality of life. Studies have suggested that cognitive impairment interacts with cardiovascular diseases such as coronary heart disease, abnormal blood pressure, heart failure, and arrhythmia. On one hand, cognitive impairment in the elderly influences the progression and self-management of cardiovascular diseases and increases the risk of cardiovascular-related adverse events. On the other hand, coronary heart disease, heart failure, higher blood pressure variability, orthostatic hypotension, and atrial fibrillation may aggravate cognitive impairment. The role of blood pressure levels on cognition remains controversial. Several shared biological pathways have been proposed as the underlying mechanism for the association. Cardiovascular diseases may lead to cognitive decline even dementia through cerebral perfusion damage, brain structural changes, inflammation, β-amyloid deposition, and neuroendocrine disorders. It is of great significance to study the interaction and put forward effective interventions in an overall perspective to reduce care burden and improve the quality of life of the elderly patients.

Background Neuropilin1 (NRP1) participates in cancer cell proliferation, migration, and metastasis as a multifunctional co‐receptor by interacting with multiple signal pathways, but few studies have addressed the precise function of NRP1 in pancreatic cancer (PACA) cells. We aimed to study whether NRP1 gene silencing involved in the proliferation and migration of PACA cells in vitro. Methods A lentiviral vector expressing NRP1 shRNA was constructed and transfected into human PACA cells (CFPAC‐1 and PANC‐1). The expression of NRP1 protein and mRNA was detected by Western blot and quantitative real‐time polymerase chain reaction (qRT‐PCR) assay, respectively. CCK‐8 assay, wound healing assay, and transwell assay were conducted to examine the effect of NRP1 silencing on cells proliferation and migration capability. Results Results of qRT‐PCR and Western blot showed successfully established, stably transfected shRNA‐NRP1 cells in PACA cells. The proliferation capacity of PACA cells in NRP1 shRNA group was lower significantly than that in the negative control (NC) group (P < .05). The invasion and migration capability of PACA cells in NRP1 shRNA group was lower significantly than that in the NC group (P < .01). Conclusions NRP1‐shRNA lentiviral interference vectors can effectively decrease NRP1 gene expression in PACA cells, thereby inhibiting cells proliferation and migration, which provides a basis for finding a valuable therapeutic target for PACA therapy.