This overlap between PD and AD suggests that common pathological pathways exist for the two diseases.
Since there may be significant potential in therapies targeting the novel pathological pathways, it is crucial to understand the molecular mechanisms involved in cardiac pathophysiology, especially ones specifically operated in the hearts.
In general, our state understanding of the pathological pathways and our knowledge of the range of possible effects of any given low molecular weight drug on these complex networks of pathways is quite superficial.
Thus, a certain basal CTGF expression might have a beneficial effect on cardiac performance while long-term CTGF upregulation leads to "overstimulation" and activation of pathological pathways resulting in loss of cardiomyocytes and ventricular dilatation.
This trigger may involve different pathological pathways including the effects of molecules acting as pathological chaperones, as well as seeding events (defined as involvement of exogenous nuclei to bypass the slow nucleation event), both homologous and heterologous.
Although in the past years there has been considerable progress in our understanding of the pathological pathways that contribute to sepsis and septic shock, pharmacological interventions are currently limited to insulin and activated protein C [7].
These interactions control processes involved in both normal and pathological pathways, which include signal transduction, cell adhesion, cellular proliferation, growth, differentiation, viral self-assembly, programmed cell death and cytoskeleton structure (for a review refer to [3]).
Phytochemicals may control several pathological pathways.
Multiple pathological pathways contribute to the final phenotype of PE.
Rodents and humans have remarkably similar genomes and share closely related biochemical, physiological and pathological pathways.
Use of these tools, therefore, opens new avenues for uncovering physiological and pathological pathways.
