Role of Heat Shock Protein 27 in Modulating Atherosclerotic Inflammation

Heat Shock Protein 27 Is an Emerging Predictor of Contrast-Induced Acute Kidney Injury on Patients Subjected to Percutaneous Coronary Interventions

“…It was demonstrated in animal models that acute ischemic kidney damage induces a 12-fold increase of HSP27 expression in the kidney tissues with a peak level observed 6 h post-reperfusion [12]. It suggests a protective role of HSP27 against hypoxia and oxidative stress [8][9][10]12,15,25]. The evidence exists that this chaperone protein inhibits apoptosis in IRI models [7].…”

“…High levels of HSP27 are normally present in the renal medulla in response to conditions of hypoxia and oxydative stress. Evidence exists that HSP27 prevents injury and restores normal cellular function in the kidney following IRI [8][9][10][11][12][13][14][15]. The association between HSP27 and CI-AKI, however, has not been elucidated.…”

Sex differences in COVID-19 mortality: opportunity to develop HSP27 (HSPB1) immunotherapy to treat hyper-inflammation?

“…Moreover, based on the assumption that ovarian hormones may be protective, a small clinical trial has begun in men > 18 years and women > 55 years with confirmed or suspected COVID-19, randomizing subjects to a transdermal patch containing estradiol or placebo (Estrogen Patch for COVID-19 Symptoms n.d.). With this in mind, we now postulate that heat shock protein 27 (HSP27), recently recognized to have potent antiinflammatory effects (Inia and O'Brien 2020), may also have a role in the treatment of COVID-19.…”

At elevated temperatures, heat shock protein genes show altered ratios of different RNAs and expression of new RNAs, including several novel HSPB1 mRNAs encoding HSP27 protein isoforms

“…The essential function of these proteins is to serve as molecular chaperones that maintain numerous cellular proteins in their normal three-dimensional structures, in order to continue performing their normal functions when the ambient temperature is increased (1)(2)(3). However, the majority of heat shock proteins also have numerous other functions and are often overexpressed in various situations of cellular stress (1,2,(4)(5)(6)(7). For example, when normal cells evolve into cancer cells, the expression of HSPs is often increased, which is usually a mechanism by which cancer cells become resistant to various therapies (5,7).…”