Neferine Attenuates Aging-Related Liver Dysfunction by Suppressing Cellular Aging via Mitochondrial Reactivation.

Cellular aging causes declining cell functionality, gradually disrupting cellular homeostasis. Mitochondria are crucial in numerous metabolic processes, including the electron transport chain and fatty acid β-oxidation. Mitochondrial dysfunction is closely linked to aging-related liver dysfunction because it impairs fatty acid metabolism, potentially leading to nonalcoholic fatty liver disease.

Kuanoniamine C Suppresses Adipogenesis and White Adipose Tissue Expansion by Modulating Mitochondrial Function.

Obesity is characterized by the excessive accumulation of fat to adipose tissue, which is related to abnormal increasing white adipose tissue (WAT) in the body, and it upregulates the risk of multiple diseases. Here, kuanoniamine C, which is a pyridoacridine alkaloid, suppressed the differentiation of pre-adipose cells into white adipocytes via the modulation of mitochondrial function, and inhibited WAT expansion in the early phase of high-fat-diet-induced obesity model. Pharmacological analysis revealed that inhibition of mitochondrial respiratory complex II, which new target of kuanoniamine C, activated reactive oxygen species (ROS)-extracellular signal-regulated kinase (ERK)-β-catenin signaling, and this signaling was antagonized by insulin-, IBMX-, and dexamethasone-induced adipogenesis.

Malonate induces the browning of white adipose tissue in high-fat diet induced obesity model.

Obesity increases the risk of various diseases, and many studies have examined prevention and treatment strategies. Browning of white adipocytes promotes triglyceride (TG) metabolism and is the new focus for treating obesity. This study investigated the role of malonate-a modulator of mitochondrial function-in adipocyte browning, and its potential as a therapeutic agent in obesity.

Restoration of mitochondrial function by polysaccharide via upregulated SOD2 in aging fibroblasts.

Reactive oxygen species (ROS), such as superoxide, are crucial factors involved in the stimulation of cellular aging. Mitochondria, which are important organelles responsible for various metabolic processes in cells, produce ROS. These ROS impair mitochondrial function, thereby accelerating aging-related cellular dysfunction.

Lotus germ extract rejuvenates aging fibroblasts via restoration of disrupted proteostasis by the induction of autophagy.

Cell aging attenuates cellular functions, resulting in time-dependent disruption of cellular homeostasis, which maintains the functions of proteins and organelles. Mitochondria are important organelles responsible for cellular energy production and various metabolic processes, and their dysfunction is strongly related to the progression of cellular aging. Here we demonstrate that disruption of proteostasis attenuates mitochondrial function before the induction of DNA damage signaling by proliferative and replicative cellular aging.