Extended Data Fig. 4: Klf9 deficiency accelerates heart failure and mitochondrial senescence with aging.
From: Klf9 is essential for cardiac mitochondrial homeostasis
a, Representative gross morphology of 24-month-old Ctrl and Klf9-CKO mice. b, Left, B- and M-mode echocardiographic analysis of 12-month-old Ctrl and Klf9-CKO mice. Right, Quantitative data showing the changes of FS, EF and LV mass (n = 6). c, Ratios of hearts or lungs weight to tibia length of 12-month-old Ctrl and Klf9-CKO mice (n = 6). d, Left, WGA staining of 12-month-old Ctrl and Klf9-CKO hearts. Right, Quantitative data for cardiomyocyte CSA (n = 6). e, Left, Masson’s trichrome staining of 12-month-old Ctrl and Klf9-CKO hearts. Right, Quantification of blue-staining replacement fibrosis (n = 6). f, Left, TUNEL staining of 12-month-old Ctrl and Klf9-CKO hearts. Right, Quantitative data for apoptosis positive cells (n = 6). g, TEM of 12-month-old Ctrl and Klf9-CKO hearts. h, i, Quantitative data of mitochondrial size distribution (h) and content (i, n = 6) based on TEM images. j, Quantification of mitochondrial protein content of 12-month-old Ctrl and Klf9-CKO hearts (n = 20). k-m, Left, Flow cytometric analysis of size (FSC) (k), transmembrane electrical potential (DiOC6) (l) and ROS production (MitoSOX) (m) of isolated cardiac mitochondria from 12-month-old Ctrl and Klf9-CKO hearts. Right, Quantitative data of FSC, DiOC6 and MitoSOX intensity (n = 6). n, qRT-PCR analysis of expression levels of genes involved in mitochondrial biogenesis in 12-month-old Ctrl and Klf9-CKO hearts (n = 6). o, Left, Western blotting analysis of proteins involved in the mitochondrial unfolded protein response (mtUPR) in 12-month-old Ctrl and Klf9-CKO hearts. Right, Quantification of AFG3L2, LONP1 and HSP60 protein levels (n = 3). Data are shown as mean ± SEM; 2-tailed Student’s t test (b, c, d, e, f, i, j, k, l, m, n, o).
