SRSF4-Associated ca-circFOXP1 Regulates Hypoxia-Induced PASMC Proliferation by the Formation of R Loop With Host Gene.

Background: Pulmonary hypertension (PH) is a rare and fatal disease, the pathological changes of which include pulmonary arterial smooth muscle cell (PASMC) proliferation, which is the pathological basis of pulmonary vascular remodeling. Studies have demonstrated that chromatin-associated circRNA can regulate a variety of biological processes, including PASMC proliferation in patients with hypoxic PH. However, the role of chromatin-associated circRNA in the proliferation of PH remains largely unexplored.

Exonic CircGUCY1A2 inhibits pulmonary artery smooth muscle cells phenotypic switching via regulating O-glycosylation of COL3A1 in pulmonary hypertension.

Pulmonary hypertension (PH) is a fatal disease characterized by pulmonary vascular remodeling, whose regulatory mechanisms remain unclear. Circular RNAs (circRNAs) are a unique class of RNA molecules produced by covalent linkages via back-splicing of linear RNA and play vital roles in regulating physiological and pathological processes. However, the dysregulation of circRNAs and their underlying mechanisms in PH remain unclear.

5-Methylcytosine-modified circRNA-CCNL2 regulates vascular remdeling in hypoxic pulmonary hypertension through binding to FXR2.

Pulmonary hypertension (PH) is a malignant cardiovascular disease with a complex etiology. 5-Methylcytosine (m5C) is a post-transcriptional RNA modification identified in both stable and highly abundant RNAs, with a lower frequency of occurrence in circular RNAs (circRNAs). Nevertheless, the function of m5C-modified circRNAs in the pathogenesis of PH remains uncertain.

CircSSR1 regulates pyroptosis of pulmonary artery smooth muscle cells through parental protein SSR1 mediating endoplasmic reticulum stress.

Introduction: Pyroptosis, inflammatory necrosis of cells, is a programmed cell death involved in the pathological process of diseases. Endoplasmic reticulum stress (ERS), as a protective stress response of cell, decreases the unfold protein concentration to inhibit the unfold protein agglutination. Whereas the relationship between endoplasmic reticulum stress and pyroptosis in pulmonary hypertension (PH) remain unknown.

Endonuclear Circ-calm4 regulates ferroptosis via a circR-Loop of the COMP gene in pulmonary artery smooth muscle cells.

Pulmonary hypertension (PH) is a serious pulmonary vascular disease characterized by vascular remodeling. Circular RNAs (CircRNAs) play important roles in pulmonary hypertension, but the mechanism of PH is not fully understood, particularly the roles of circRNAs located in the nucleus. Circ-calmodulin 4 (circ-calm4) is expressed in both the cytoplasm and the nucleus of pulmonary arterial smooth muscle cells (PASMCs).

Correction: Positive Feedback-Loop of Telomerase Reverse Transcriptase and 15-Lipoxygenase-2 Promotes Pulmonary Hypertension.

[This corrects the article DOI: 10.1371/journal.pone.

CircNAP1L4 regulates pulmonary artery smooth muscle cell proliferation via the NAP1L4-mediated super-enhancer-driven glycolysis gene hexokinase II (HK II) in pulmonary hypertension.

Glycolysis is a major determinant of pulmonary artery smooth muscle cell (PASMC) proliferation in pulmonary hypertension (PH). Circular RNAs (circRNAs) are powerful regulators of glycolysis in multiple diseases; however, the role of circRNAs in glycolysis in PH has been poorly characterized. The aim of this study was to uncover the regulatory mechanism of a new circRNA, circNAP1L4, in human pulmonary artery smooth muscle cell (HPASMC) proliferation through the host protein NAP1L4 to regulate the super-enhancer-driven glycolysis gene hexokinase II (HK II).

CircLMBR1 inhibits phenotypic transformation of hypoxia-induced pulmonary artery smooth muscle via the splicing factor PUF60.

Phenotypic transformation of pulmonary artery smooth muscle cells (PASMCs) contributes to vascular remodeling in hypoxic pulmonary hypertension (PH). Recent studies have suggested that circular RNAs (circRNAs) may play important roles in the vascular remodeling of hypoxia-induced PH. However, whether circRNAs cause pulmonary vascular remodeling by regulating the phenotypic transformation in PH has not been investigated.

SP1 undergoes phase separation and activates RGS20 expression through super-enhancers to promote lung adenocarcinoma progression.

Lung adenocarcinoma (LUAD) is the leading cause of cancer-related death worldwide, but the underlying molecular mechanisms remain largely unclear. The transcription factor (TF) specificity protein 1 (SP1) plays a crucial role in the development of various cancers, including LUAD. Recent studies have indicated that master TFs may form phase-separated macromolecular condensates to promote super-enhancer (SE) assembly and oncogene expression.

Presenilin 1 Is a Therapeutic Target in Pulmonary Hypertension and Promotes Vascular Remodeling.

Small muscular pulmonary artery remodeling is a dominant feature of pulmonary arterial hypertension (PAH). PSEN1 affects angiogenesis, cancer, and Alzheimer's disease. We aimed to determine the role of PSEN1 in the pathogenesis of vascular remodeling in pulmonary hypertension (PH).

Glucosylglycerol phosphorylase, a potential novel pathway of microbial glucosylglycerol catabolism.

Glucosylglycerol (GG) is a natural compatible solute that can be synthesized by many cyanobacteria and a few heterotrophic bacteria under high salinity conditions. In cyanobacteria, GG is synthesized by GG-phosphate synthase and GG-phosphate phosphatase, and a hydrolase GGHA catalyzes its degradation. In heterotrophic bacteria (such as some Marinobacter species), a fused form of GG-phosphate phosphatase and GG-phosphate synthase is present, but the cyanobacteria-like degradation pathway is not available.

Efficient flocculation pretreatment of coal gasification wastewater by halophilic bacterium Halovibrio variabilis TG-5.

The isolated halophilic bacterial strain Halovibrio variabilis TG-5 showed a good performance in the pretreatment of coal gasification wastewater. With the optimum culture conditions of pH = 7, a temperature of 46 °C, and a salinity of 15%, the chemical oxygen demand and volatile phenol content of pretreated wastewater were decreased to 1721 mg/L and 94 mg/L, respectively. The removal rates of chemical oxygen demand and volatile phenol were over 90% and 70%, respectively.

Super Enhancer-Associated Circular RNA-CircKrt4 Regulates Hypoxic Pulmonary Artery Endothelial Cell Dysfunction in Mice.

Background: Circular RNAs (circRNAs) have been implicated in pulmonary hypertension progression through largely unknown mechanisms. Pulmonary artery endothelial cell (PAEC) dysfunction is a hallmark in the pathogenesis of pulmonary hypertension. However, the specific role of circular RNAs in PAEC injury caused by hypoxia remains unclear.

Circ-myh8 Promotes Pulmonary Hypertension by Recruiting KAT7 to Govern Hypoxia-Inducible Factor-1α Expression.

Background Aberrant expression of circular RNAs (circRNAs) contributes to the initiation and progression of pulmonary hypertension (PH). Hypoxia-inducible factor (HIF) is a well-known modulator of hypoxia-induced PH. The role and underlying mechanism of circRNAs in the regulation of HIF expression remains elusive.

Circ-calm4 regulates hypoxia-induced pulmonary artery smooth muscle autophagy by binding Purb.

Pulmonary hypertension (PH) is a serious and fatal disease characterized by pulmonary vasoconstriction and pulmonary vascular remodeling. The excessive autophagy of pulmonary artery smooth muscle cells (PASMCs) is one of the important factors of pulmonary vascular remodeling. A number of studies have shown that circular RNA (circRNA) can participate in the onset of PH.

[Role of non-coding RNAs in vascular smooth muscle cell calcification].

Vascular calcification, the deposition of calcium in the arterial wall, is often linked to increased stiffness of the vascular wall. Vascular calcification is one of the important factors for high morbidity and mortality of cardiovascular and cerebrovascular diseases, as well as an important biomarker in atherosclerotic cardiovascular events, stroke and peripheral vascular diseases. The mechanism of vascular calcification has not been fully elucidated.

LncRNA FENDRR with m6A RNA methylation regulates hypoxia-induced pulmonary artery endothelial cell pyroptosis by mediating DRP1 DNA methylation.

Background: Pyroptosis is a form of programmed cell death involved in the pathophysiological progression of hypoxic pulmonary hypertension (HPH). Emerging evidence suggests that N6-methyladenosine (m6A)-modified transcripts of long noncoding RNAs (lncRNAs) are important regulators that participate in many diseases. However, whether m6A modified transcripts of lncRNAs can regulate pyroptosis in HPH progression remains unexplored.

RPS4XL encoded by lnc-Rps4l inhibits hypoxia-induced pyroptosis by binding HSC70 glycosylation site.

Pyroptosis is involved in pulmonary hypertension (PH); however, whether this process is regulated by long non-coding RNAs (lncRNAs) is unclear. Some lncRNAs encode peptides; therefore, whether the regulation of pyroptosis in PH depends on lncRNAs themselves or their encoded peptides needs to be explored. We aimed to characterize the role of the peptide RPS4XL encoded by lnc-Rps4l and its regulatory mechanisms during pyroptosis in PH.

From formic acid to single-cell protein: genome-scale revealing the metabolic network of Paracoccus communis MA5.

With the increase in population growth and environmental pollution, the daily protein supply is facing great challenges. Single-cell protein (SCP) produced by microorganism fermentation is a good alternative for substituting plant- and animal-derived proteins. In this study, Paracoccus communis MA5 isolated from soil previously demonstrated an excellent ability to synthesize SCP directly from sodium formate.