Tissue-engineered smooth muscle cell and endothelial progenitor cell bi-level cell sheets prevent progression of cardiac dysfunction, microvascular dysfunction, and interstitial fibrosis in a rodent model of type 1 diabetes-induced cardiomyopathy

Table 1 Echocardiographic data

	0 (Pre-DM induction)	4 weeks (Pre-treatment)	6 weeks (2 weeks after treatment)	8 weeks (4 weeks after treatment)
FS (%)
Control	47.0 ± 3.6	49.8 ± 3.5	50.9 ± 2.7	48.8 ± 2.1
Untreated DMCM	46.3 ± 2.2	38.8 ± 2.3	37.9 ± 2.7	35.1 ± 3.0
Treated DMCM	46.3 ± 3.1	39.5 ± 2.2	42.7 ± 3.3	42.6 ± 3.5
Group effect: P < 0.0001; time effect: P < 0.0001; interaction group × time effect: P < 0.0001
LVEDD (mm)
Control	6.338 ± 0.497	6.477 ± 0.481	6.711 ± 0.276	6.694 ± 0.359
Untreated DMCM	6.471 ± 0.456	7.173 ± 0.327	7.705 ± 0.341	7.965 ± 0.320
Treated DMCM	6.273 ± 0.379	7.114 ± 0.414	7.405 ± 0.352	7.483 ± 0.635
Group effect: P < 0.0001; time effect: P < 0.0001; interaction group × time effect: P < 0.05
LVEDD (mm)
Control	3.368 ± 0.449	3.262 ± 0.449	3.305 ± 0.268	3.427 ± 0.268
Untreated DMCM	3.477 ± 0.315	4.416 ± 0.306	4.786 ± 0.309	4.786 ± 0.362
Treated DMCM	3.373 ± 0.330	4.305 ± 0.348	4.242 ± 0.347	4.300 ± 0.550
Group effect: P < 0.0001; time effect: P < 0.0001; interaction group × time effect: P < 0.0001

Serial data for fraction shortening (%), left ventricle end-diastolic dimension (mm), and left ventricle end-systolic dimension (mm) were demonstrated
DM diabetes mellitus, DMCM diabetic cardiomyopathy, FS fraction shortening, LVEDD left ventricle end-systolic dimension, LVESD left ventricle end-systolic dimension

ISSN: 1475-2840