Mitochondrial dynamics in pulmonary disease: Implications for the potential therapeutics.

Mitochondria are dynamic organelles that continuously undergo fusion/fission to maintain normal cell physiological activities and energy metabolism. When mitochondrial dynamics is unbalanced, mitochondrial homeostasis is broken, thus damaging mitochondrial function. Accumulating evidence demonstrates that impairment in mitochondrial dynamics leads to lung tissue injury and pulmonary disease progression in a variety of disease models, including inflammatory responses, apoptosis, and barrier breakdown, and that the role of mitochondrial dynamics varies among pulmonary diseases. These findings suggest that modulation of mitochondrial dynamics may be considered as a valid therapeutic strategy in pulmonary diseases. In this review, we discuss the current evidence on the role of mitochondrial dynamics in pulmonary diseases, with a particular focus on its underlying mechanisms in the development of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), asthma, pulmonary fibrosis (PF), pulmonary arterial hypertension (PAH), lung cancer and bronchopulmonary dysplasia (BPD), and outline effective drugs targeting mitochondrial dynamics-related proteins, highlighting the great potential of targeting mitochondrial dynamics in the treatment of pulmonary disease.

Modeling Impacts of Urbanization on Winter Boundary Layer Meteorology and Aerosol Pollution in the Central Liaoning City Cluster, China.

The influence of urbanization on the frequent winter aerosol pollution events in Northeast China is not fully understood. The Weather Research and Forecasting Model with Chemistry (WRF-Chem) coupled with urban canopy (UC) models was used to simulate the impact of urbanization on an aerosol pollution process in the Central Liaoning city cluster (CLCC), China. To investigate the main mechanisms of urban expansion and UC on the winter atmospheric environment and the atmospheric diffusion capacity (ADC) in the CLCC, three simulation cases were designed using land-use datasets from different periods and different UC schemes. A comparative analysis of the simulation results showed that the land-use change (LU) and both LU and UC (LUUC) effects lead to higher surface temperature and lower relative humidity and wind speed in the CLCC by decreasing surface albedo, increasing sensible heat flux, and increasing surface roughness, with a spatial distribution similar to the distribution of LU. The thermal effect leads to an increase in atmospheric instability, an increase in boundary layer height and diffusion coefficient, and an increase in the ADC. The LU and LUUC effects lead to a significant decrease in near-surface PM2.5 concentrations in the CLCC due to changes in meteorological conditions and ADC within the boundary layer. The reduction in surface PM2.5 concentrations due to the LU effect is stronger at night than during daytime, while the LUUC effect leads to a greater reduction in surface PM2.5 concentrations during the day, mainly due to stronger diffusion and dilution caused by the effect of urban turbulence within different levels caused by the more complex UC scheme. In this study, the LU and LUUC effects result in greater thermal than dynamic effects, and both have a negative impact on surface PM2.5 concentrations, but redistribute pollutants from the lower urban troposphere to higher altitudes.

The role of mitochondrial dynamics in disease.

Mitochondria are multifaceted and dynamic organelles regulating various important cellular processes from signal transduction to determining cell fate. As dynamic properties of mitochondria, fusion and fission accompanied with mitophagy, undergo constant changes in number and morphology to sustain mitochondrial homeostasis in response to cell context changes. Thus, the dysregulation of mitochondrial dynamics and mitophagy is unsurprisingly related with various diseases, but the unclear underlying mechanism hinders their clinical application. In this review, we summarize the recent developments in the molecular mechanism of mitochondrial dynamics and mitophagy, particularly the different roles of key components in mitochondrial dynamics in different context. We also summarize the roles of mitochondrial dynamics and target treatment in diseases related to the cardiovascular system, nervous system, respiratory system, and tumor cell metabolism demanding high-energy. In these diseases, it is common that excessive mitochondrial fission is dominant and accompanied by impaired fusion and mitophagy. But there have been many conflicting findings about them recently, which are specifically highlighted in this view. We look forward that these findings will help broaden our understanding of the roles of the mitochondrial dynamics in diseases and will be beneficial to the discovery of novel selective therapeutic targets.