Forensic pathologists are routinely confronted with unclear causes of death or related findings. In some instances, difficulties arise in relation to questions posed by criminal investigators or prosecutors. Such scenarios may include questions about wound vitality or cause of death where typical or landmark findings are difficult to ascertain. In addition to the usual examinations required to clarify unclear causes of death or address specific questions, immunohistochemistry and genetic analyses have become increasingly important techniques in this area since their establishment last century. Since then, many studies have determined the usefulness and significance of immunohistochemical and genetic investigations on cellular structures and proteins. For example, these proteins include heat shock proteins (Hsp), which were first described in 1962 and are so called based on their molecular weight. They predominantly act as molecular chaperones with cytoprotective functions that support cell survival under (sub) lethal conditions. They are expressed in specific cellular compartments and have many divergent functions. Central family members include, Hsp 27, 60, and 70. This mini review investigates recent research on the Hsp family, their application range, respective forensic importance, and current limitations and provides an outlook on possible applications within forensic science.

In developed countries, sudden infant death syndrome (SIDS) is the leading cause of death in infants in their first year of life. The risk of SIDS is increased if parents smoked during pregnancy and in presence of the child. Glutathione S-transferases (GSTs) catalyse the conjugation of glutathione with electrophilic compounds and toxins, making them less reactive and easier to excrete. As a gene dose effect was observed for GSTM1 and GSTT1, the aim of this study was to investigate whether there is a connection between homozygous or heterozygous gene deletions of GSTM1 or GSTT1 and the occurrence of SIDS. We found that heterozygous deletion of GSTM1 occurred significantly more frequently in the SIDS case group compared to the control group. A homozygous deletion of GSMT1 was slightly more frequently in the control group. A homozygous gene deletion of GSTT1 showed no significant difference between the SIDS group and the control group. We also found that in the SIDS group, the number of victims that were exposed to cigarette smoke was significantly higher than the number of victims without cigarette smoke exposure and that the mean lifetime of children whose mothers smoked was shorter in comparison with non-smoking mothers. In SIDS cases with homozygous gene deletions of GSTM1, the median life span of children with tobacco smoke exposure was 60 days shorter than without smoke exposure. In conclusion, the absence of these two genes is not the only trigger for SIDS but could be a critical aspect of SIDS aetiology, particularly in SIDS cases with smoking parents.