Broadly neutralizing antibodies derived from the earliest COVID-19 convalescents protect mice from SARS-CoV-2 variants challenge.

Coronavirus disease 2019 (COVID-19) was first reported three years ago, when a group of individuals were infected with the original SARS-CoV-2 strain, based on which vaccines were developed. Here, we develop six human monoclonal antibodies (mAbs) from two elite convalescents in Wuhan and show that these mAbs recognize diverse epitopes on the receptor binding domain (RBD) and can inhibit the infection of SARS-CoV-2 original strain and variants of concern (VOCs) to varying degrees, including Omicron strains XBB and XBB.1.

Huangkui capsule attenuates diabetic kidney disease through the induction of mitophagy mediated by STING1/PINK1 signaling in tubular cells.

Background: Mitochondria is critic to tubulopathy, especially in diabetic kidney disease (DKD). Huangkui capsule (HKC; a new ethanol extract from the dried corolla of Abelmoschus manihot) has significant clinical effect on DKD. Previous studies have shown that HKC protects kidney by regulating mitochondrial function, but its mechanism is still unclear.

Hyodeoxycholic acid attenuates cholesterol gallstone formation via modulation of bile acid metabolism and gut microbiota.

Background & Aims: Hyodeoxycholic acid (HDCA), a hydrophilic bile acid (BA), may prevent and suppress the formation of cholesterol gallstones (CGs). However, the mechanism by which HDCA prevents CGs formation remains unclear. This study aimed to investigate the underlying mechanism of HDCA in preventing CG formation.

NF-B regulates brown adipocyte function through suppression of ANT2.

The transcription factor nuclear factor of kappa-light-chain-enhancer of activated B cells (NF-B) is expressed in brown adipocytes, but its role remains largely unknown in the cells. This issue was addressed in current study by examining NF-B in brown adipocytes and . NF-B activity was increased by differentiation of brown adipocytes through elevation of p65 (RelA) expression.

Photolytic Removal of Red Blood Cell Membranes Camouflaged on Nanoparticles for Enhanced Cellular Uptake and Combined Chemo-Photodynamic Inhibition of Cancer Cells.

Biomimetic therapeutics offer great potential for drug delivery that avoids immune recognition. However, the coated cell membrane usually hinders the cellular uptake of nanoparticles; thus, structure-changeable formulations have attracted increasing attention. Herein, we report photolytic pyropheophorbide a (PA)-inserted red blood cell (RBC) membrane-camouflaged curcumin dimeric prodrug (CUR-TK)-poly(lactic--glycolic acid) (PLGA) nanoparticles [(CUR-TK)-PLGA@RBC-PA] for enhanced cancer therapy.

High doses of butyrate induce a reversible body temperature drop through transient proton leak in mitochondria of brain neurons.

Aims: Sodium butyrate (SB) is a major product of gut microbiota with signaling activity in the human body. It has become a dietary supplement in the treatment of intestinal disorders. However, the toxic effect of overdosed SB and treatment strategy remain unknown.

[Novel role of intracellular ATP in obesity pathology].

ATP is an important energy source for cells. Traditionally, intracellular ATP levels are believed to be relatively stable and will not rise consistently in the physiological conditions. However, new studies suggest that ATP levels may rise in multiple tissues under the condition of energy surplus contributing to the metabolic disorders in obesity.

ATP reduces mitochondrial MECR protein in liver of diet-induced obese mice in mechanism of insulin resistance.

Mitochondrial 2-enoyl-acyl-carrier protein reductase (MECR) is an enzyme in the mitochondrial fatty acid synthase (mtFAS) pathway. MECR activity remains unknown in the mechanism of insulin resistance in the pathogenesis of type 2 diabetes. In the present study, MECR activity was investigated in diet-induced obese (DIO) mice.

Sodium butyrate opens mitochondrial permeability transition pore (MPTP) to induce a proton leak in induction of cell apoptosis.

Induction of apoptosis is a strategy in the treatment of glioma, a malignant tumor with the highest prevalence in the brain. Sodium butyrate (NaB) induces apoptosis in glioma cells at pharmacological dosages (>2.5 mM), but the mechanism remains largely unknown beyond the mitochondrial potential drop.

Cigarette smoke extract increases mitochondrial membrane permeability through activation of adenine nucleotide translocator (ANT) in lung epithelial cells.

Cigarette smoke is one of major risk factors in the pathogenesis of chronic obstructive pulmonary disease (COPD). It is generally believed that cigarette smoke induces mitochondrial damage in the alveolar epithelial cells to contribute to COPD. However, the exact molecular mechanism remains unknown for the mitochondrial damage.

Protective effect of ISO‑1 against advanced glycation end product aggravation of PC12 cell injury induced by Aβ1‑40.

Advanced glycation end products (AGEs) are important pathogenic substances involved in diabetes mellitus (DM) and its complications. AGEs also serve important roles in promoting the development of Alzheimer's disease (AD). Macrophage migration inhibitory factor (MIF), an inflammatory stimulant and a pathogenic factor involved in DM, was previously reported to be present at increased levels in the cerebrospinal fluid of patients with AD and mild cognitive impairment compared with age‑matched healthy controls.

Reduction of mitochondrial 3-oxoacyl-ACP synthase (OXSM) by hyperglycemia is associated with deficiency of α-lipoic acid synthetic pathway in kidney of diabetic mice.

LA (alpha-Lipoic acid) deficiency represents a risk factor in the pathogenesis of diabetic complications as synthetic LA is routinely used in the treatment of the complications in patients. The mechanism underlying LA deficiency remains elusive in the diabetic conditions. In the present study, we investigated the synthetic pathway of LA in both type 1 and 2 diabetic mice.