Dual-specificity phosphatases (DUSPs) serve critical roles in the regulation of mitogen-activated protein kinases, but their functions in the cardiovascular system remain poorly defined. Here, we provide evidence that DUSP5, which resides in the nucleus and specifically dephosphorylates extracellular signal-regulated kinase (ERK1/2), blocks pulmonary vascular smooth muscle cell proliferation. In response to angiotensin II infusion, mice lacking DUSP5 develop pulmonary hypertension and right ventricular cardiac hypertrophy. The findings illustrate DUSP5-mediated suppression of ERK signaling in the lungs as a protective mechanism.

中文翻译：

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DUSP5 介导的平滑肌细胞增殖抑制抑制肺动脉高压和右心室肥大

双特异性磷酸酶 (DUSP) 在丝裂原活化蛋白激酶的调节中起着关键作用，但它们在心血管系统中的功能仍未明确。在这里，我们提供证据表明 DUSP5 位于细胞核中并特异性地使细胞外信号调节激酶 (ERK1/2) 去磷酸化，从而阻止肺血管平滑肌细胞增殖。作为对血管紧张素 II 输注的反应，缺乏 DUSP5 的小鼠会出现肺动脉高压和右心室心肌肥厚。这些发现表明 DUSP5 介导的肺部 ERK 信号抑制是一种保护机制。