Fig. 6

Transcriptional changes in blood after death. a Multi-Dimensional Scaling of blood samples shows separation between pre and post-mortem samples. Samples are colored by the Hardy scale of the cause of death. b Number of genes differentially expressed between the pre-mortem samples and the post-mortem samples stratified at different PMI intervals. Darker filling corresponds to genes that are found as differentially expressed in the previous interval. c The five main temporal patterns of change in functional activities upon organismic death. d Hypoxia seems to play a major role in the pre-to post-mortem transcription as reflected in the way in which the carbohydrate metabolism is affected (activations in red, deactivations in blue). Response to hipoxia is activated from pathways “Platelet activation pathway” and “cGMP-PKG signaling pathway” through the activation of the corresponding circuits that end in the effector gene ITPR1, annotated as Response to hypoxia, and from pathways “HIF-1 signaling pathway” and “cGMP-PKG signaling pathway” through the activation of the effector gene VEGFA. The “HIF-1 signaling pathway” also activates Glycolysis through the activation of different circuits that trigger effector proteins (PDK1, PFKL, ALDOA, etc.) with annotations such as glycolytic process, canonical glycolysis, glucose metabolic process, etc. The “HIF-1 signaling pathway” also inhibits Tricarboxylic acid cycle through the inhibition of circuits that trigger the effector protein PDHA1 with diverse GO annotations such as tricarboxylic acid cycle, acetyl-CoA biosynthetic process from pyruvate or carbohydrate metabolic process