24 research outputs found
Additional file 1 of Evaluation of the effect of tofogliflozin on the tissue characteristics of the carotid wall—a sub-analysis of the UTOPIA trial
Additional file 1: Tables S1. Between-group comparison of changes in clinical parameters during the treatment period. Table S2. Changes in concomitantly used anti-diabetic agents. Table S3. Changes in concomitantly used cardiovascular medications. Table S4. The changes of GSM-CCA on the basis of tertiles of changes in mean-IMT during observation perio
Study Protocol for the Initial Choice of DPP-4 Inhibitor in Japanese Patients with Type 2 diabetes Mellitus: Effect of Linagliptin on QOL (INTEL-QOL) Trial
<p></p><p><b>Article full text</b></p><p><br></p><p>The full text of this article can
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Rationale and Design for the J-DISCOVER Study: DISCOVERing the Treatment Reality of Type 2 Diabetes in a Real-World Setting in Japan—A Protocol
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A Real-World Data of the Incidence of Macrovascular Complications in Japanese Patients with Type 2 Diabetes: The Sitagliptin Registration Type 2 Diabetes-Juntendo Collaborating Project
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The Influence of Sitagliptin on Treatment-Related Quality of Life in Patients with Type 2 Diabetes Mellitus Receiving Insulin Treatment: A Prespecified Sub-Analysis
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The Effect of Linagliptin versus Metformin Treatment-Related Quality of Life in Patients with Type 2 Diabetes Mellitus
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Protocol of a Prospective Observational Study on the Relationship Between Glucose Fluctuation and Cardiovascular Events in Patients with Type 2 Diabetes
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Characteristics according to quintile categories of type 1 life style pattern score.
<p>Characteristics according to quintile categories of type 1 life style pattern score.</p
Defective autophagy in vascular smooth muscle cells enhances cell death and atherosclerosis
<p>Macroautophagy/autophagy is considered as an evolutionarily conserved cellular catabolic process. In this study, we aimed to elucidate the role of autophagy in vascular smooth muscle cells (SMCs) on atherosclerosis. SMCs cultured from mice with SMC-specific deletion of the essential autophagy gene <i>atg7</i> (<i>Atg7cKO</i>) showed reduced serum-induced cell growth, increased cell death, and decreased cell proliferation rate. Furthermore, 7-ketocholestrerol enhanced apoptosis and the expression of CCL2 (chemokine [C-C motif] ligand 2) with the activation of TRP53, the mouse ortholog of human and rat TP53, in SMCs from <i>Atg7cKO</i> mice. In addition, <i>Atg7cKO</i> mice crossed with <i>Apoe</i> (apolipoprotein E)-deficient mice (<i>apoeKO; Atg7cKO:apoeKO</i>) showed reduced medial cellularity and increased TUNEL-positive cells in the descending aorta at 10 weeks of age. Intriguingly, <i>Atg7cKO: apoeKO</i> mice fed a Western diet containing 1.25% cholesterol for 14 weeks showed a reduced survival rate. Autopsy of the mice demonstrated the presence of aortic rupture. Analysis of the descending aorta in <i>Atg7cKO:apoeKO</i> mice showed increased plaque area, increased TUNEL-positive area, decreased SMC-positive area, accumulation of macrophages in the media, and adventitia and perivascular tissue, increased CCL2 expression in SMCs in the vascular wall, medial disruption, and aneurysm formation. In conclusion, our data suggest that defective autophagy in SMCs enhances atherosclerotic changes with outward arterial remodeling.</p
