Cross-talk between bioactive lipid mediators and the unfolded protein response in ischemic stroke

Ischemic cerebral stroke is a severe medical condition that affects about 15 million people every year and is the second leading cause of death and disability globally. Ischemic stroke results in neuronal cell death and neurological impairment. Current therapies may not adequately address the deleterious metabolic changes and may increase neurological damage. Oxygen and nutrient depletion along with the tissue damage result in endoplasmic reticulum (ER) stress, including the Unfolded Protein Response (UPR), and neuroinflammation in the affected area and cause cell death in the lesion core. The spatio-temporal production of lipid mediators, either pro-inflammatory or pro-resolving, decides the course and outcome of stroke. The modulation of the UPR as well as the resolution of inflammation promotes post-stroke cellular viability and neuroprotection. However, studies about the interplay between the UPR and bioactive lipid mediators remain elusive and this review gives insights about the crosstalk between lipid mediators and the UPR in ischemic stroke. Overall, the treatment of ischemic stroke is often inadequate due to lack of effective drugs, thus, this review will provide novel therapeutical strategies that could promote the functional recovery from ischemic stroke.

Automated summary

Hypoxia and tissue damage lead to endoplasmic reticulum stress and neuroinflammation, causing neuronal cell death and neurological impairment in ischemic stroke. Modulating endoplasmic reticulum stress and inflammation can enhance cell survival and protect neurons in ischemic stroke. The interplay between lipid mediators and endoplasmic reticulum stress plays a crucial role in the progression and outcome of ischemic stroke.