Heat shock protein 27 as a neuroprotective biomarker and a suitable target for stem cell therapy and pharmacotherapy in ischemic stroke

Abstract

Ischemic stroke is a major common cause of death and long‐term disability worldwide. Several pathophysiological events including excitotoxicity, oxidative/nitrative stress, inflammation, and apoptosis are involved in ischemic injuries. Recently, the molecular mechanisms involved in cerebral ischemia through a focus on a member of small heat shock proteins family, Hsp27, has been developed. Notably, following exposure to ischemia, Hsp27 expression in the brain could be increased rather than the normal condition and it may play an important role in neuroprotection after ischemic stroke. The neuroprotection effects of Hsp27 may arise from its anti‐oxidant, anti‐inflammatory, anti‐apoptotic, and chaperonic properties. Moreover, some therapeutic strategies such as stem cell therapy and pharmacotherapy have been developed with Hsp27 targeting. In this review, we describe the function and structure of Hsp27 and its possible role in neuroprotection after ischemic stroke. Finally, we present current studies in stroke therapy, which focused on Hsp27 targeting.

Acupuncture protects against cerebral ischemia–reperfusion injury via suppressing endoplasmic reticulum stress-mediated autophagy and apoptosis

“…Ischemic stroke is a major type of stroke, which results in death and long-term disability worldwide (Behdarvandy et al 2019 ). Rapid restoration of cerebral blood flow is the preferred treatment method for ischemic stroke (Schregel et al 2018 ).…”

Revolutionizing Stroke Recovery: Unveiling the Promise of Stem Cell Therapy

“… 36 Additionally, stem cells secrete growth factors and cytokines that promote neuroprotection, angiogenesis, and neurogenesis, thereby creating a more favorable environment for brain repair. 37 They also modulate the immune response to the injury, reducing inflammation, which is a critical factor in limiting further damage post-stroke. 38 Furthermore, stem cells can facilitate synaptic plasticity and neural network reorganization, essential for restoring functional deficits caused by the stroke.…”

Fabry disease: Mechanism and therapeutics strategies

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