Autophagy in pulmonary hypertension: Emerging roles and therapeutic implications

Autophagy is an important mechanism for cellular self‐digestion and basal homeostasis. This gene‐ and modulator‐regulated pathway is conserved in cells. Recently, several studies have shown that autophagic dysfunction is associated with pulmonary hypertension (PH). However, the relationship between autophagy and PH remains controversial. In this review, we mainly introduce the effects of autophagy‐related genes and some regulatory molecules on PH and the relationship between autophagy and PH under the conditions of hypoxia, monocrotaline injection, thromboembolic stress, oxidative stress, and other drugs and toxins. The effects of other autophagy‐related drugs, such as chloroquine, 3‐methyladenine, rapamycin, and other potential therapeutic drugs and targets, in PH are also described. Autophagic dysfunction is associated with pulmonary hypertension (PH). However, the relationship between autophagy and PH remains controversial. In this review, we mainly introduce the effects of autophagy‐related genes and some regulatory molecules on PH and the relationship between autophagy and PH under the conditions of hypoxia, monocrotaline injection, thromboembolic stress, oxidative stress, and other drugs and toxins.