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. 2023 Jun 7;30(7):1786–1798. doi: 10.1038/s41418-023-01179-0

Fig. 4. TMEM11 overexpression inhibits cardiomyocytes proliferation and cardiac regeneration in neonatal hearts.

Fig. 4

a Representative images of haematoxylin-eosin stained transverse sections of WT and TMEM11 transgenic (TMEM11 Tg) adult mice hearts (Bar = 2 mm). b Heart to body weight ratio in WT and TMEM11 Tg adult mice hearts (n = 7 mice per group). c The left ventricular fractional shortening (FS%) in WT and TMEM11 Tg adult mice hearts (n = 7 mice per group). d Cardiomyocytes surface area was measured in WT and TMEM11 Tg adult mice hearts (n = 6 mice per group). e Quantification of the number of Ki67-positive cardiomyocytes in WT and TMEM11 Tg heart sections at 7 days after birth (n = 6 mice per group). f Representative confocal images and qualification of pH3-positive cardiomyocytes (red, Bar = 25 μm) in WT and TMEM11 Tg heart sections at 7 days after birth (n = 6 mice per group). (g–i) WT and TMEM11 Tg neonatal mice (P1) were subjected to MI. g Quantification of pH3-positive and Ki67-positive cardiomyocytes in heart sections at 7 days after MI (n = 6 mice per group). h Analysis of the percentage of the fibrotic area (n = 8 mice per group). i Echocardiography analysis of fractional shortening (FS, n = 7 mice per group) at P7 post-MI. Data are presented as the mean ± s.d. Two-sided Student’s t test (b–i) was performed.