Pulmonary hypertension (PH) is a clinical and pathophysiological syndrome caused by changes in pulmonary vascular structure or function that results in increased pulmonary vascular resistance and pulmonary arterial pressure, and it is characterized by pulmonary endothelial dysfunction, pulmonary artery media thickening, pulmonary vascular remodeling, and right ventricular hypertrophy, all of which are driven by an imbalance between the growth and death of pulmonary vascular cells. Programmed cell death (PCD), different from cell necrosis, is an active cellular death mechanism that is activated in response to both internal and external factors and is precisely regulated by cells. More than a dozen PCD modes have been identified, among which apoptosis, autophagy, pyroptosis, ferroptosis, necroptosis, and cuproptosis have been proven to be involved in the pathophysiology of PH to varying degrees. This article provides a summary of the regulatory patterns of different PCD modes and their potential effects on PH. Additionally, it describes the current understanding of this complex and interconnected process and analyzes the therapeutic potential of targeting specific PCD modes as molecular targets.

Introduction: The present study systematically reviewed the clinical features and risk factors in patients undergoing maintenance hemodialysis (MHD) who also acquired coronavirus disease 2019 (COVID-19). More specifically, clinical manifestations, prognosis, and risk factors for death among this population were explored. Method: A literature search using the PubMed, Web of Science, and Embase databases, for articles involving patients with laboratory-confirmed COVID-19 and undergoing MHD published between January 1, 2020, and March 13, 2022, was performed. Random-effects meta-analyses were performed to calculate the weighted mean prevalence and corresponding 95% confidence interval (CI) or weighted means and 95% CI. Heterogeneity among studies was assessed using I² statistics. Results: Twenty-two studies including 13,191 patients with COVID-19 undergoing MHD were selected. The most common symptoms included fever (53% [95% CI 41%–65%]) and cough (54% [95% CI 48%-60%]); however, 17% (95% CI 11%–22%) of the cases were asymptomatic. In subgroup analysis, the proportion of male patients (65% [95% CI 58%–71%]), and patients with coronary artery disease (30% [95% CI 17%–44%) and chronic obstructive pulmonary disease (9% [95% CI 4%–15%]) was greater in the non-survivor group compared with the survivor group. Furthermore, patients undergoing MHD, who were also positive for COVID-19, exhibited a high mortality rate (24% [95% CI 19%–28%]). Conclusions: MHD patients with COVID-19 may initially present as asymptomatic or with mild symptoms; nevertheless, in this study, these patients exhibited a higher risk for death compared with COVID-19 patients not undergoing MHD. Moreover, male sex and underlying cardiovascular and respiratory diseases increased the mortality risk.

The changes of microbiota in lungs could change interleukin-17a (IL-17a) expression by altering microRNAs (miRNAs) profile, thus contributing to the pathogenesis of chronic obstructive pulmonary disease (COPD). In this study, we aimed to study molecular mechanisms’ underlying effect of microbiota imbalance on COPD deterioration. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were performed to analyze expression of miRNAs and IL-17a mRNA. ELISA was used to evaluate abundance of IL-17a in plasma, peripheral blood monocyte, and sputum of COPD mice and patients. Luciferase assay was performed to explore underlying molecular mechanisms. The expression of miR-122, miR-30a, and miR-99b were remarkably decreased in COPD mice, while the expression of IL-17a was notably increased in plasma, peripheral blood monocytes, and lung tissues of COPD mice. The levels of Lactobacillus/Moraxella and IL-17a expression were significantly enhanced in sputum of exacerbated COPD patients, along with notably decreased expression of miR-122 and miR-30a. Luciferase assay confirmed that miR-122 and miR-30a played an inhibitory role in IL-17a expression. We identified miR-122 and miR-30a as differentially expressed miRNAs in sputum and plasma of COPD patients in exacerbation-month12 group. Furthermore, downregulated miR-122 and miR-30a expression associated with microbiota imbalance may contribute to COPD deterioration by enhancing IL-17a production.

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic respiratory disease characterized by peripheral distribution of bilateral pulmonary fibrosis that is more pronounced at the base. IPF has a short median survival time and a poor prognosis. Therefore, it is necessary to identify effective prognostic indicators to guide the treatment of patients with IPF.