The 60 kDa heat shock protein (HSP60) is a chaperone essential for mitochondrial proteostasis ensuring thus sufficient aerobic energy production. In pathological conditions, HSP60 can be translocated from the mitochondria and excreted from the cell. In turn, the extracellular HSP60 has a strong ability to trigger and enhance inflammatory response with marked pro-inflammatory cytokine induction, which is mainly mediated by toll-like receptors binding. Previous studies have found increased circulating levels of HSP60 in hypertensive patients, as well as enhanced HSP60 expression and membrane translocation in the hypertrophic myocardium. These observations are of particular interest as they could provide a possible pathophysiological explanation of the severe course and worse outcome of SARS-CoV-2 infection in hypertensive patients, repeatedly reported during recent COVID-19 pandemic, and related to hyperinflammatory response and cytokine storm development during the third phase of the disease. In this regard, pharmacological inhibition of HSP60 could attract attention to potentially ameliorate inappropriate inflammatory reaction in severe COVID-19 patients. Among HSP60 antagonizing drugs, mizoribine is the most intriguing, since it is clinically approved and exerts antiviral activity. However, this topic requires to be further scrutinized.

中文翻译：

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COVID-19和高血压：HSP60是导致严重病程和预后不良的元凶吗？

60 kDa热休克蛋白（HSP60）是线粒体蛋白稳态所必需的分子伴侣，可确保产生足够的有氧能量。在病理条件下，HSP60可从线粒体易位并从细胞中排出。反过来，细胞外HSP60具有强烈的触发和增强炎症反应的能力，并具有明显的促炎细胞因子诱导作用，这主要是由toll样受体结合介导的。先前的研究发现，高血压患者的HSP60循环水平增加，肥厚型心肌中HSP60的表达和膜移位增强。这些观察特别有趣，因为它们可以为高血压患者SARS-CoV-2感染的严重病程和较差的结局提供可能的病理生理学解释，在最近的COVID-19大流行期间反复报道，并与疾病第三阶段的高炎症反应和细胞因子风暴发展有关。在这方面，HSP60的药理抑制作用可能引起人们的注意，以减轻严重的COVID-19患者潜在的不适当的炎症反应。在HSP60拮抗药物中，米佐列滨是最吸引人的，因为它已被临床批准并发挥抗病毒活性。但是，这个主题需要进一步审查。在HSP60拮抗药物中，米佐列滨是最吸引人的，因为它已被临床批准并发挥抗病毒活性。但是，这个主题需要进一步审查。在HSP60拮抗药物中，米佐列滨是最吸引人的，因为它已被临床批准并发挥抗病毒活性。但是，这个主题需要进一步审查。