Fig.Ā 1From: Endothelium-specific deletion of p62 causes organ fibrosis and cardiac dysfunctionEndothelium knockout of p62 induces cardiac dysfunction in mice. A Generation of endothelium-specific knockout mice for p62. B Identification of genes in the tail of mice. Tek-Cre mutant: 300Ā bp.p62 mutant: 525Ā bp.Wild type:400Ā bp. Mice within the red frame were the p62Endo mouse we needed. C The immunofluorescence co localization of endothelial markers CD31 (green) and p62 (red) in lung tissue. D Echocardiography analysis in mice. E Assessment of systolic and diastolic parameters including ventricular septal thickness, left ventricular diameter, and left ventricular posterior wall thickness in mice. F Measurement of heart rate in mice. G Evaluation of systolic, diastolic, and mean arterial pressure in mice. H Calculation of ejection fraction and shortening fraction in mice. I Analysis of left ventricular systolic and diastolic end volume in mice. J Determination of left ventricular mass in mice. K Monitoring of body weight changes in mice. * pā<ā0.05 and ** pā<ā0.01Back to article page