The pathogenic mechanisms of many diseases are well understood at the molecular level, but there are prevalent syndromes associated with pathogenic signaling, such as diabetes and chronic inflammation, where our understanding is more limited. Here, we report that pathogenic signaling suppresses the mobility of a spectrum of proteins that play essential roles in cellular functions known to be dysregulated in these chronic diseases. The reduced protein mobility, which we call proteolethargy, was linked to cysteine residues in the affected proteins and signaling-related increases in excess reactive oxygen species. Diverse pathogenic stimuli, including hyperglycemia, dyslipidemia, and inflammation, produce similar reduced protein mobility phenotypes. We propose that proteolethargy is an overlooked cellular mechanism that may account for various pathogenic features of diverse chronic diseases.

中文翻译：

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蛋白瘤是慢性病的一种致病机制


许多疾病的致病机制在分子水平上已得到很好的理解，但存在与致病性信号相关的普遍综合征，例如糖尿病和慢性炎症，我们对这些疾病的理解更加有限。在这里，我们报道了致病性信号转导抑制了一系列蛋白质的移动性，这些蛋白质在已知在这些慢性疾病中失调的细胞功能中起着重要作用。蛋白质迁移率降低，我们称之为蛋白营养素，与受影响蛋白质中的半胱氨酸残基和过量活性氧的信号相关增加有关。不同的致病刺激，包括高血糖、血脂异常和炎症，产生类似的蛋白质迁移率降低表型。我们提出蛋白瘤是一种被忽视的细胞机制，它可能解释了各种慢性疾病的各种致病特征。