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. Author manuscript; available in PMC: 2022 Nov 15.
Published in final edited form as: Circ Res. 2021 Oct 6;129(11):1021–1035. doi: 10.1161/CIRCRESAHA.121.319482

Figure 3. Cilp1-inactivation protects mice against pathological cardiac remodeling.

Figure 3.

(A-E) Cilp1 KO and WT mice were subjected to MI. (A) fractional shortening (FS%), (B) LVESD, and (C) LVEDD of mice at Sham and post-MI day 3, 7, & 14 (n=5–10). (D) Representative images of Masson’s Trichrome-stained transverse cross sections of post-MI day 14 hearts at the levels indicated. (E) Infarct size was quantified from sections shown in D and normalized to cross-section area. (F-M) Cilp1 KO and WT littermates were subjected to Sham (S) or TAC (T) surgery. Hearts were harvested 6 weeks later. (F) FS%, (G) LVESD, (H) LVEDD, (I) HW/BW, (J) cardiomyocyte (CM) area, (K-M) relative mRNA of fetal genes (K) and Periostin (Postn) (L) of sham and TAC WT and Cilp1 KO mouse hearts. (M) Fibrotic area (%) of WT and Cilp1 KO hearts after 6 weeks of sham and TAC. Error bars are SEM, * p<0.05 by student t test.