Cellular stress response

As expected, such cells were also highly vulnerable to stress, and ceased to be viable at elevated temperature ranges.

[citation needed] Indeed, if a cell under normal (meaning unstressed) conditions has denatured proteins artificially injected into it, it will trigger a stress response.

[3] Other toxins that either directly or indirectly lead to the release of free radicals can generate misfolded proteins.

Chronic ER stress produces endogenous or exogenous damage to cells and activates UPR, which leads to impaired intracellular calcium and redox homeostasis.

[11] Cancer cells may become dependent on stress response mechanisms that involve lysosomal macromolecule degradation, or even autophagy that recycles entire organelles [12] However, tumor cells exhibit therapeutic stress resistance-associated secretory phenotype involving extracellular vesicles (EVs) such as oncosomes and heat shock proteins.

[14] Early research has suggested that cells which are better able to synthesize stress proteins and do so at the appropriate time are better able to withstand damage caused by ischemia and reperfusion.

Cells subjected to heat shock. Cells in slide 'e' exhibit dysmorphic nuclei as a result of this exposure to stress, however 24 hours later cells largely recovered, as shown in slide 'f'.