About the Special Issue

Sublethal hypoxic or ischemic events can improve the tolerance of not only cells or tissues, but also of entire organs, to subsequent hypoxic or ischemic harmful episode. This phenomenon is called ischemic preconditioning. The terms preconditioning and tolerance were first used in this context in the 1960s. In addition, a variety of physical and pharmacological stimuli can also induce ischemic tolerance. While its clinical use is still lacking, tolerance has been speculated to play a protective role in cerebral ischemia. From this date, a plethora of studies contributed to the identification of the molecular mechanisms underlying ischemic tolerance.

In this respect, various forms of pretreatment stimulation can trigger endogenous protection or regeneration mechanisms through various signaling molecules and pathways, thus triggering an early or delayed adaptive response.

The early adaptation is thought to be a consequence of alterations in ionic homeostasis, ion channel permeability, protein phosphorylation, and other post-translational modifications. In contrast, delayed ischemic preconditioning, known as ‘classical preconditioning’, requires gene activation and de novo protein synthesis. This manifests itself only hours to days following preconditioning and involves both the inhibition of detrimental mechanisms or increase in survival and repair mechanisms.

With this special issue, we would like to participate to the general investigation on the molecular pathways determining tolerance with particular emphasis to the ionic mechanisms.

Keywords: ischemic tolerance; calcium homeostasis; calcium storing organelles; ER stress; autophagy; neurodegeneration

Call for Papers