线粒体分裂在肺动脉高压肺血管重构中的作用

Role of mitochondrial fission in vascular remodeling in pulmonary hypertension

肺动脉高压(pulmonary hypertension,PH)是一类以肺血管阻力进行性升高为主要特征的疾病,其发病率约为每年2.0~7.6/100万,患病率则为11~26/100万[1]。PH致残、致死率高,预后差,是目前心血管疾病治疗的难点之一[1]。目前治疗PH的药物包括L型钙离子通道拮抗剂、磷酸二酯酶抑制剂、可溶性鸟苷酸环化酶激动剂、内皮素受体拮抗剂和前列环素激动剂。上述药物主要针对肺血管收缩,而对于PH发病中最重要的环节--肺血管重构的作用有限[1-2]。

Pulmonary hypertension(PH)is characterized by sustained vasoconstriction and progressive obliteration of small-resistance pulmonary arteries.Current therapies for PH have limited effect,and the prognosis of patients with PH is poor.Pulmonary vascular remodeling is the key pathological feature of PH.However,the precise pathophysiological mechanism of pulmonary vascular remodeling is not fully elucidated.Recent studies have indicated that increased mitochondrial fission is closely associated with pulmonary vascular remodeling.In this review,we summarize the present evidence implicating the role of mitochondrial fission in PH,and provide potential therapeutic strategies targeting mitochondrial fission to improve outcome of the patients with PH.