Abstract
Lipofuscin is an intracellular aggregate of highly oxidized proteins that cannot be digested in the ubiquitin-proteasome system and accumulate mainly in lysosomes, especially in aged cells and pathological conditions. However, no systematic study has evaluated the cardiac accumulation of lipofuscin during human ageing and sudden cardiac death (SCD). Age estimation in unidentified bodies and postmortem SCD diagnosis are important themes in forensics. Thus, we aimed to elucidate their correlations with myocardial lipofuscin accumulation. We collected 76 cardiac samples from autopsy patients aged 20–97 years. After histopathological examination, myocardial lipofuscin was measured using its autofluorescence. Lipofuscin accumulated mainly in the perinuclear zone, and its accumulation rate positively correlated with chronological ageing (r = 0.82). Meanwhile, no significant change in lipofuscin level was observed with different causes of death, including SCD. There was also no significant change in lipofuscin level in relation to body mass index, serum brain natriuretic peptide level, or heart weight. Moreover, we performed LC3 and p62 immunoblotting to evaluate autophagic activity, and no change was observed in ageing. Therefore, lipofuscin accumulation more directly reflects chronological ageing rather than human cardiac pathology. Our study reveals the stability and utility of cardiac lipofuscin measurement for age estimation during autopsy.
Highlights
Lipofuscin is a yellow-brown pigment composed of highly oxidized proteins, lipids, and metals[1,2,3]
Subjects were divided into seven groups according to the cause of death: accident (Acc), ischemic heart failure (IHF), hypertrophic heart failure (HHF), cancer (Ca), brain haemorrhage (Br), hepatic failure (Hep), and other diseases (Dis)
There were no significant differences in age, body mass index (BMI), and serum brain natriuretic peptide (BNP) level among the groups
Summary
Lipofuscin is a yellow-brown pigment composed of highly oxidized proteins, lipids, and metals[1,2,3]. Intracellular lipofuscin interferes with the ubiquitin-proteasome system and autophagy-lysosomal pathway[8,14,19]. These clearance systems are essential for the removal of damaged organelles and oxidized proteins, and impairment in these systems could exacerbate lipofuscin accumulation and reduce cellular viability[10,20]. Age prediction trials have been performed using pulp/tooth volume, telomere length, and DNA methylation patterns[28,29,30]. We have analysed the myocardial lipofuscin accumulations in various causes of death including SCD, the major cause of sudden internal death. Lipofuscin quantification can be worthy of trial in forensics
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