High level of lactate dehydrogenase and ischaemia-reperfusion injury regulate the multiple organ dysfunction in patients with COVID-19.

BACKGROUND: Multiple organ damage has been observed in patients with COVID-19, but the exact pathway is not known. Vital organs of the human body may get affected after replication of SARS-CoV-2, including the lungs, heart, kidneys, liver and brain. It triggers severe inflammation and impairs the function of two or more organ systems. Ischaemia-reperfusion (IR) injury is a phenomenon that can have disastrous effects on the human body. METHODS: In this study, we analysed the laboratory data of 7052 hospitalised patients with COVID-19 including lactate dehydrogenase (LDH). A total of 66.4% patients were men and 33.6% were women, which indicated gender difference as a prominent factor to be considered. RESULTS: Our data showed high levels of inflammation and elevated markers of tissue injury from multiple organs C reactive protein, white blood cell count, alanine transaminase, aspartate aminotransferase and LDH. The number of red blood cells, haemoglobin concentration and haematocrit were lower than normal which indicated a reduction in oxygen supply and anaemia. CONCLUSION: On the basis of these results, we proposed a model linking IR injury to multiple organ damage by SARS-CoV-2. COVID-19 may cause a reduction in oxygen towards an organ, which leads to IR injury.

Competing Endogenous RNA Regulatory Networks of hsa_circ_0126672 in Pathophysiology of Coronary Heart Disease.

Coronary heart disease (CHD) is a global health concern, and its molecular origin is not fully elucidated. Dysregulation of ncRNAs has been linked to many metabolic and infectious diseases. This study aimed to explore the role of circRNAs in the pathogenesis of CHD and predicted a candidate circRNA that could be targeted for therapeutic approaches to the disease. circRNAs associated with CHD were identified and CHD gene expression profiles were obtained, and analyzed with GEO2R. In addition, differentially expressed miRNA target genes (miR-DEGs) were identified and subjected to functional enrichment analysis. Networks of circRNA/miRNA/mRNA and the miRNA/affected pathways were constructed. Furthermore, a miRNA/mRNA homology study was performed. We identified that hsa_circ_0126672 was strongly associated with the CHD pathology by competing for endogenous RNA (ceRNA) mechanisms. hsa_circ_0126672 characteristically sponges miR-145-5p, miR-186-5p, miR-548c-3p, miR-7-5p, miR-495-3p, miR-203a-3p, and miR-21. Up-regulation of has_circ_0126672 affected various CHD-related cellular functions, such as atherosclerosis, JAK/STAT, and Apelin signaling pathways. Our results also revealed a perfect and stable interaction for the hybrid of miR-145-5p with NOS1 and RPS6KB1. Finally, miR-145-5p had the highest degree of interaction with the validated small molecules. Henchashsa_circ_0126672 and target miRNAs, notably miR-145-5p, could be good candidates for the diagnosis and therapeutic approaches to CHD.

Free Fatty Acid Overload Targets Mitochondria: Gene Expression Analysis of Palmitic Acid-Treated Endothelial Cells.

Lipotoxicity is known to cause cellular dysfunction and death in non-adipose tissue. A major cause of lipotoxicity is the accumulation of saturated free fatty acids (FFA). Palmitic acid (PA) is the most common saturated fatty acid found in the human body. Endothelial cells form the blood vessels and are the first non-adipose cells to encounter FFA in the bloodstream. FFA overload has a direct impact on metabolism, which is evident through the changes occurring in mitochondria. To study these changes, the PA-treated human coronary artery endothelial cell (HCAEC) dataset was obtained from the Gene Expression Omnibus (GEO), and it was analyzed to obtain differentially expressed genes (DEGs) from the nucleus and mitochondria. Functional and pathway enrichment analyses were performed on DEGs. Results showed that nuclear and mitochondrial DEGs were implicated in several processes, e.g., reactive oxygen species (ROS) production, mitochondrial fusion and fission, Ca2+ sequestering, membrane transport, the electron transport chain and the process of apoptosis. To better understand the role of FFA in endothelial cell damage, these DEGs can lead to future experiments based on these findings.