Abstract：
Cardiovascular disease (CVD) is the primary cause of morbidity and mortality in the Western world. Multiple molecular and cellular processes underpinning the pathogenesis of CVD are regulated by the zinc finger transcription factor and product of an immediate-early gene, early growth response-1 (Egr-1). Egr-1 regulates multiple pro-inflammatory processes that underpin the manifestation of CVD. The activity of Egr-1 itself is influenced by a range of post-translational modifications including sumoylation, ubiquitination and acetylation. Egr-1 also undergoes phosphorylation by protein kinases, such as extracellular-signal regulated kinase (ERK) which is itself phosphorylated by MEK. This article reviews recent progress on the MEK-ERK-Egr-1 cascade, notably regulation in conjunction with factors and agents such as TET2, TRIB2, MIAT, SphK1, cAMP, teneligliptin, cholinergic drugs, red wine and flavonoids, wogonin, febuxostat, docosahexaenoic acid and AT1R blockade. Such insights should provide new opportunity for therapeutic intervention in CVD.
摘要：
心血管疾病（CVD）是西方世界发病率和死亡率的主要原因。支持CVD发病机理的多个分子和细胞过程受锌指转录因子和立即早期基因产物的调节，早期生长反应-1（Egr-1）。Egr-1调节支持CVD表现的多种促炎过程。Egr-1本身的活性受到一系列翻译后修饰的影响，包括sumoylation，泛素化和乙酰化。Egr-1也通过蛋白激酶进行磷酸化，例如细胞外信号调节激酶(ERK),其本身被MEK磷酸化。本文综述了MEK-ERK-Egr-1级联反应的最新进展。特别是与TET2、TRIB2、MIAT等因子和试剂结合的调节，SphK1,cAMP,teneligliptin,胆碱能药物，红酒和类黄酮，Wogonin,非布索坦,二十二碳六烯酸和AT1R阻断。这些见解应该为CVD的治疗干预提供新的机会。
