Lipofuscin is widely regarded as an indicator of ageing. The amount of intracellular lipofuscin increases with age and the rate of accumulation is inversely correlated with longevity [[1], [2], [3], [4], [5]]. The accumulation of lipofuscin has been widely studied in post-mitotic cells, especially in long-lived cells such as neurons and cardiomyocytes [6,7]. Lipofuscin is believed to accumulate in cells after mitosis because it is non-degradable and cannot be removed by exocytosis [8,9]. However, some studies have suggested that lipofuscin may be removed from normal nerve cells through the capillary endothelium [10,11]. After treatment with cyclodextrin for 4–6 weeks, chromatosomes become embedded in the endothelium or lumen of myocardial capillaries and are removed through the bloodstream [12]. Bulging protuberances on the endothelial surface of human coronary arteries may contain lipofuscin and eventually detach and enter the bloodstream [13]. However, whether lipofuscin can be removed from tissues remains unclear and requires further study [14].

To confirm that the elimination and transport of lipofuscin is a normal physiological phenomenon in animal myocardium, we investigated the migration and fate of lipofuscin in the rat heart. We found that some cardiomyocytes could expel lipofuscin into the interstitium, which would then enter the bloodstream by several methods.