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From: Deletion of the Lmna gene in fibroblasts causes senescence-associated dilated cardiomyopathy by activating the double-stranded DNA damage response and induction of senescence-associated secretory phenotype

Deletion of the <i>Lmna </i>gene in fibroblasts causes senescence-associated dilated cardiomyopathy by activating the double-stranded DNA damage response and induction of senescence-associated secretory phenotype

Figure 3. Gross phenotype and survival. (A) Gross morphology of the WT, Pdgfra-Cre, Pdgfra-Cre:Lmna^W/F, and Pdgfra-Cre:Lmna^F/F mice at six weeks of age. (B) Growth curves of the mice in the experimental groups up to six weeks of age. (C) Kaplan-Meier survival plots show the survival rates up to ~2 months of age, the longest survival time of the Pdgfra-Cre:Lmna^F/F mice. (D) Kaplan-Meier survival plots show the survival rates up to 20 months of age. Log-rank test p-value is shown. (E-G) Heart weight (E), body weight (F), and heart weight to body weight ratio (HW/BW) of the WT, Pdgfra-Cre, Pdgfra-Cre:Lmna^W/F, and Pdgfra-Cre:Lmna^F/F mice at six weeks of age. (H) Wheat Germ Agglutinin (WGA) stained thin myocardial sections used to calculate myocyte cross-sectional area (CSA). I. Graph representing myocyte CSA indexed to heart weight (CSAI) in the control and experimental groups.

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Committee on Publication Ethics

Portico

Committee on Publication Ethics

Portico