Skip to main content
. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Int J Biochem Cell Biol. 2012 Jun 15;44(10):1632–1645. doi: 10.1016/j.biocel.2012.06.006

Figure 4.

Figure 4

Small HSPs and cardiac stress. (A–B) Description of experimental cardiac stresses. (A) Ischemia procedure is shown with the indications for the area of infarction (AOI) corresponding to dead cardiac cells and area at risk (AAR) corresponding to cardiac cells which have experienced the interruption of blood supply (ischemia) before being reperfused. (B) Transaortic constriction (TAC) which increased cardiac work load is schematized. (C) Mouse models of modified sHSP expression were submitted to various protocols of ischemia and reperfusion as illustrated in A. The area of infarction (AOI) to area at risk (AAR) ratio was calculated for HSF1 TG (Zou et al., 2003), hHSPB1 TG (2lines: TG18 and TG24) Efthymiou et al., 2004), HspB2/5 DKO (AMI, acute myocardial infarction; PI, preconditioned infarction) (Benjamin et al., 2007), rHspB5 (Ray et al., 2001), HspB6 TG (Fan et al., 2005), HspB8 TG (Depre et al., 2006). Schematic graph was prepared based on the data referenced above where the ratio values for the experimental animal model (white bar) are presented as relative to the values obtained with wild-type (WT) animals (black bar). (D) Cardiac hypertrophy is measured by the ratio heart weight/body weight (HW/BW). Schematic graph was prepared using published data where the variation of HW/BW in experimental animal models (white bar) is presented as relative to WT ones (black bar), under normal conditions or after transaortic constriction (TAC) as shown in (B). The data are compiled for HSF1 TG (Sakamoto et al., 2006), HSF1 KO (Zou et al., 2011), HspB1(Zhang et al., 2010) HspB2/5 DKO and HSPB5 TG (Kumarapeli et al., 2010), HSPB8 TG (Depre et al., 2002), HSPB8 KO (Qiu et al., 2011).