Background/Aims: Activation of stromal interaction molecule 1 (STIM1) and Orai1 participates in the development of cardiac hypertrophy. Store-operated Ca²⁺ entry-associated regulatory factor (SARAF) is an intrinsic inhibitor of STIM1-Orai1 interaction. Thus, we hypothesized that SARAF could prevent cardiac hypertrophy. Methods: Male C57BL/6 mice, aged 8 weeks, were randomly divided into sham and abdominal aortic constriction surgery groups and were infected with lentiviruses expressing SARAF and GFP (Lenti-SARAF) or GFP alone (Lenti-GFP) via intramyocardial injection. At 4 weeks after aortic constriction, left ventricular structure and function were assessed by echocardiography and hemodynamic assays. The gene and protein expressions of SARAF, STIM1, and Orai1 were measured by quantitative PCR and Western blot, respectively. Results: Gene and protein expressions of SARAF were significantly decreased, while STIM1 and Orai1 were increased in the heart tissue compared with sham group. Overexpression of SARAF in the heart prevented the upregulation of STIM1 and Orai1, and importantly, attenuated aortic constriction-induced decrease in maximal rate of left ventricular pressure decay and increases in thickness of interventricular septum and left ventricular posterior wall, heart weight/body weight ratio, and size of cardiomyocytes. Blood pressure detected through the carotid artery and left ventricular systolic function were not affected by SARAF overexpression. In addition, overexpression of SARAF also attenuated angiotensin II-induced upregulation of STIM1 and Orai1 and hypertrophy of cultured cardiomyocytes. Conclusion: Overexpression of SARAF in the heart prevents cardiac hypertrophy, probably through suppressing the upregulation of STIM1/Orai1.

To determine whether computed tomography perfusion imaging (CTPI)-derived parameters are associated with vascular cognitive impairment (VCI) in patients with transient ischemic attack (TIA). Patients with first-time anterior circulation TIA (diagnosed within 24 h of onset) and normal cognition, treated between August 2009 and August 2014 at the Department of Neurology of Chengdu Military General Hospital, China, were analyzed retrospectively. Patients underwent whole-brain CTPI within 1 week of TIA to detect cerebral blood volume (CBV), cerebral blood flow (CBF), mean transit time (MTT) and time to peak (TTP) in the ischemic region. Based on cognitive function assessment 4 weeks after TIA, using the Montreal cognitive assessment (MoCA) and mini mental state examination, the patients were divided into control and VCI groups. CTPI parameters and other clinical data were compared between groups, and Spearman's correlation analysis used to identify associations between cognitive scores and CTPI parameters in the VCI group. 50 patients (25 per group; aged 55-72 years) were included. Patient age, gender, smoking status, alcohol consumption, educational level, time from TIA onset to admission, time from TIA onset to CTPI, and prevalence of hypertension, diabetes mellitus, hyperlipidemia, atrial fibrillation and hyperhomocysteinemia did not differ between groups. Both groups showed TTP and MTT prolongation, CBF reduction, but no change in CBV in the ischemic region; these changes were significantly larger in the VCI group (P < 0.05). MTT correlated negatively with MoCA score (r = -0.51, P = 0.009). CTPI could facilitate early diagnosis of VCI in patients with anterior circulation TIA.