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. 2020 Dec 3;21(23):9238. doi: 10.3390/ijms21239238

Figure 1.

Figure 1

Cisd2 delays cardiac ageing as revealed by reduced lipofuscin accumulation and preserved myocardial ultrastructure. (A) Lipofuscin deposits can be clearly identified in cardiac tissues by autofluorescence detected with 330–380 nm excitation light and 420 nm barrier filter of a confocal fluorescence microscope. The red color indicates lipofuscin and green color indicates myocardia. (B) There is a significant increase of lipofuscin accumulation during cardiac ageing of WT mice. Intriguingly, a high level of Cisd2 reduces lipofuscin accumulation in Cisd2TG mice, while Cisd2 deficiency significantly elevates lipofuscin accumulation in Cisd2KO mice. The areas of lipofuscin accumulation and the myocardia are measured using Fiji/ImageJ 1.52e (National Institutes of Health, Bethesda, MD, USA). Ten fields per subject are observed at 20× objective magnification, and the lipofuscin accumulation (lipofuscin deposit area/myocardial area) was calculated. * p < 0.05, ** p < 0.01, *** p < 0.001. (C,D) Transmission electron microscopy (TEM) analysis for the left ventricle of heart. In 24-mo WT mice (C), age-associated mitochondria degeneration, lipofuscin accumulation, and necrotic debris of degenerative myofibril and organelles are detectable and easily identified. (D) In 24-mo Cisd2TG mice, relatively normal ultrastructures, namely intact mitochondria, ER, and cardiac myofibrils, are found. (C′) (D′) Schematic presentation for ultrastructure of left ventricle shown in (C) and (D), respectively. MD: mitochondrial degeneration, Lf: lipofuscin, ND: necrotic debris of degenerative myofibril and organelles, G: Golgi apparatus, M: mitochondria, Cm: cardiac myofibril, ER: endoplasmic reticulum, N: nucleus.