Effects of Lipid Overload on Heart in Metabolic Diseases

Metabolic diseases are often associated with lipid and glucose metabolism abnormalities, which increase the risk of cardiovascular disease. Diabetic cardiomyopathy (DCM) is an important development of metabolic diseases and a major cause of death. Lipids are the main fuel for energy metabolism in the heart. The increase of circulating lipids affects the uptake and utilization of fatty acids and glucose in the heart, and also affects mitochondrial function. In this paper, the mechanism of lipid overload in metabolic diseases leading to cardiac energy metabolism disorder is discussed.

The Role of Osteoclast Energy Metabolism in the Occurrence and Development of Osteoporosis

In recent decades, the mechanism underlying bone metabolic disorders based on energy metabolism has been heavily researched. Bone resorption by osteoclasts plays an important role in the occurrence and development of osteoporosis. However, the mechanism underlying the osteoclast energy metabolism disorder that interferes with bone homeostasis has not been determined. Bone resorption by osteoclasts is a process that consumes large amounts of adenosine triphosphate (ATP) produced by glycolysis and oxidative phosphorylation. In addition to glucose, fatty acids and amino acids can also be used as substrates to produce energy through oxidative phosphorylation. In this review, we summarize and analyze the energy-based phenotypic changes, epigenetic regulation, and coupling with systemic energy metabolism of osteoclasts during the development and progression of osteoporosis. At the same time, we propose a hypothesis, the compensatory recovery mechanism (involving the balance between osteoclast survival and functional activation), which may provide a new approach for the treatment of osteoporosis.

LncRNA FENDRR Inhibits ox-LDL Induced Mitochondrial Energy Metabolism Disorder in Aortic Endothelial Cells via miR-18a-5p/PGC-1α Signaling Pathway

Atherosclerosis (AS) is the main cause of morbidity and mortality in the world. Mitochondrial dysfunction is closely related to AS. At present, several signaling pathways related to mitochondrial dysfunction have been found, one of which is around PGC-1α. PGC-1α is a transcription activator, which is related to mitochondrial biogenesis and antioxidant defense. In this study, we explored the effect of miR-18a-5p/PGC-1α signaling pathway on mitochondrial energy metabolism in HAECs with ox-LDL treatment. The results showed that the mitochondrial energy metabolism disorder in HAECs treated by ox-LDL was related to the downregulation of LncRNA FENDRR and PGC-1α. FENDRR could reverse ox-LDL induced mitochondrial energy metabolism disorder and upregulate the PGC-1α expression. FENDRR could be used as ceRNA to inhibit the miR-18a-5p expression and reduce the negative regulation of miR-18a-5p on PGC-1α. Downregulation of miR-18a-5p expression or upregulation of PGC-1α in ox-LDL treated HAECs could reverse mitochondrial energy metabolism disorder. In conclusion, these findings suggested that FENDRR/miR-18a-5p/PGC-1α signaling pathway regulated mitochondrial energy metabolism in HAECs; ox-LDL downregulated the expression of PGC-1α and cause mitochondrial energy metabolism disorder by inhibiting this signal pathway.