Chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PH) are both chronic progressive respiratory diseases that cannot be completely cured. COPD is characterized by irreversible airflow limitation, chronic airway inflammation, and gradual decline in lung function, whereas PH is characterized by pulmonary vasoconstriction, remodeling, and infiltration of inflammatory cells. These diseases have similar pathological features, such as vascular hyperplasia, arteriolar contraction, and inflammatory infiltration. Despite these well-documented observations, the exact mechanisms underlying the occurrence and development of COPD and PH remain unclear. Evidence that mitochondrial dynamics imbalance is one major factor in the development of COPD and PH. Mitochondrial dynamics is precisely regulated by mitochondrial fusion proteins and fission proteins. When mitochondrial dynamics equilibrium is disrupted, it causes mitochondrial and even cell morphological dysfunction. Mitochondrial dynamics participates in various pathological processes for heart and lung disease. Mitochondrial dynamics may be different in the early and late stages of COPD and PH. In the early stages of the disease, mitochondrial fusion increases, inhibiting fission, and thereby compensatorily increasing adenosine triphosphate (ATP) production. With the development of the disease, mitochondria decompensation causes excessive fission. Mitochondrial dynamics is involved in the development of COPD and PH in a spatiotemporal manner. Based on this understanding, treatment strategies for mitochondrial dynamics abnormalities may be different at different stages of COPD and PH disease. This article will provide new ideas for the potential treatment of related diseases.
Humans ; Mitochondrial Dynamics/physiology* ; Pulmonary Disease, Chronic Obstructive/metabolism* ; Hypertension, Pulmonary/metabolism* ; Mitochondria/metabolism* ; Animals

Objective To investigate the hospital mortality of rheumatic heart disease (RHD)and major cause of death. Methods One hundred and thirty patients with RHD prepared to take valve replacement from January 2006 to November 2009 were involved in this study. They were divided into two groups according to all clinical data: death group (10 cases ) and survival group (120 cases ). The clinical data and complications were collected, and the hospital mortality and their causes were analyzed with Logistic regression analysis. Results Univariate analysis: total bilirubin and indirect bilirubin levels in death group [(30.31 ± 19.10), (22.38 ± 17.34) μmol/L] were significantly higher than those in survival group [(19.47 ± 8.61),(12.92 ± 7.30) μmol/L] (P ＜ 0.01). The incidence of postoperative complications,history of cerebral infarction and cardiovascular complications in death group were significantly higher than those in survival group (P ＜0.01). The Logistic regression analysis showed that the postoperative complications was an independent risk factor for hospital mortality (P =0.002). Conclusions RHD with postoperative complications is identified as an independent predictor of hospital mortality. It is very important to enhance the treatment and care during hospitalization.