Piperlongumine, a -derived amide alkaloid, protects mice from ovariectomy-induced osteoporosis by inhibiting osteoclastogenesis suppression of p38 and JNK signaling.

Postmenopausal osteoporosis (PMOP) is a metabolic bone disease that results from overproduction and hyperactivation of osteoclasts caused by insufficient estrogen in women after menopause. Current therapeutic strategies are mainly focused on treating PMOP patients who have already developed severe bone loss or even osteoporotic fractures. Obviously, a better strategy is to prevent PMOP from occurring in the first place.

BMSC-Derived Exosomes Alleviate Intervertebral Disc Degeneration by Modulating AKT/mTOR-Mediated Autophagy of Nucleus Pulposus Cells.

The pathogenesis of intervertebral disc degeneration (IDD) is still unclear. It has been shown that the pathological process of IDD is most closely related to inflammation of nucleus pulposus cells (NPCs), in which inflammatory factors play an important role. Exosomes are the main paracrine mediators and are microvesicles with biological functions similar to those of the cells from which they are derived.

HDAC inhibitor quisinostat prevents estrogen deficiency-induced bone loss by suppressing bone resorption and promoting bone formation in mice.

Postmenopausal osteoporosis (PMOP) is a metabolic skeletal disorder characterized by reduced bone mass and impaired bone microarchitecture resulting in increased bone fragility and fracture risk. PMOP is primarily caused by excessive osteoclastogenesis induced by estrogen deficiency. Quisinostat (Qst) is a potent hydroxamate-based second-generation inhibitor of histone deacetylases (HDACs) that can inhibit osteoclast differentiation in vitro, and protect mice from titanium particle-induced osteolysis in vivo.

Triptolide ameliorates osteoarthritis by regulating nuclear factor kappa B-mediated inflammatory response.

Objectives: Osteoarthritis (OA) is a joint degenerative disease that commonly occurs in older people and affect the quality of life. Triptolide (TPL), a compound derived from Tripterygium wilfordii, has been shown to exhibit anti-inflammatory properties. Here, we investigated the therapeutic effect of TPL on the experimental OA as well as the underlying molecular mechanisms.

USP7 Inhibition Alleviates HO-Induced Injury in Chondrocytes via Inhibiting NOX4/NLRP3 Pathway.

Osteoarthritis (OA), the most common form of arthritis, is a very common joint disease that often affects middle-aged to elderly people. However, current treatment options for OA are predominantly palliative. Thus, understanding its pathological process and exploring its potential therapeutic approaches are of great importance.

High glucose inhibits osteogenic differentiation of bone marrow mesenchymal stem cells via regulating miR-493-5p/ZEB2 signalling.

Diabetic osteoporosis (DOP) is attributed to the aberrant physiological function of bone marrow mesenchymal stem cells (BMSCs) under high glucose (HG) environment. MicroRNAs (miRNAs) are involved in the pathological processes of DOP. We aimed to explore the underlying mechanism of miRNA in DOP.

Low-Intensity Pulsed Ultrasound Alleviates Osteoarthritis Condition Through Focal Adhesion Kinase-Mediated Chondrocyte Proliferation and Differentiation.

Objective: Osteoarthritis (OA) is a prevalent chronic multifactorial degenerative disease characterized by joint tissue inflammation, osteophyte formation, subchondral bone sclerosis, and articular cartilage degradation. Low-intensity pulsed ultrasound (LIPUS), a noninvasive ultrasound technique, is widely used to attenuate diseases. The aim of this study was to investigate whether LIPUS can ameliorate OA, and to explore its underlying molecular mechanism.

DDIT3 modulates cancer stemness in gastric cancer by directly regulating CEBPβ.

Objectives: Cancer stem cells (CSCs) have been identified to correlate with the initiation and metastasis of tumours, and DNA damage-inducible transcript 3 (DDIT3) is associated with the poor prognosis in gastric cancer (GC). However, whether DDIT3 mediates CSCs stemness in GC is still unclear.

Methods: Microarray analysis and Gene Ontology (GO) were conducted to identify the differentially expressed genes in GC tissues from GC patients.

Retracted Article: Macrophage-derived exosomes mediate osteosarcoma cell behavior by activating AKT signaling.

Osteosarcoma is the most common type of bone tumor, which severely threatens the health of adolescents and young adults. Tumor-infiltrating macrophages have been shown to mediate cancer progression extracellular vesicles. However, their potential mechanisms in osteosarcoma progression and in drug-resistance are still not yet known.

CircZNF609/miR-134-5p/BTG-2 axis regulates proliferation and migration of glioma cell.

Objectives: MicroRNAs are abundant in eukaryotic cells and play key roles in cancers. Circular RNAs (CircRNAs) served as the competing endogenous RNAs (ceRNAs) in mediating multiple cell processes. This study aims to define the role of CircRNA CircZNF609/miR-134-5p in glioma as well as the underlying regulating mechanism.

Dendritic cells aggregate inflammation in experimental osteoarthritis through a toll-like receptor (TLR)-dependent machinery response to challenges.

Aims: Dendritic cells (DCs) and Toll-like receptor (TLR) participate in mediating inflammation process. However, the functional role of TLR expressed on DCs in osteoarthritis (OA) development has not been defined yet. The purpose of this study was to investigate the role and mechanism of TLR and DCs in the progression of experimental osteoarthritis (OA).

Low dose of indomethacin and Hedgehog signaling inhibitor administration synergistically attenuates cartilage damage in osteoarthritis by controlling chondrocytes pyroptosis.

Blockade of Hedgehog signaling can prevent osteoarthritis (OA) syndromes. However, the amelioration of related inflammation condition is limited. The purpose of this study was to observe the effect of combined use of Hedgehog signaling inhibitor GANT-61 and common clinical anti-inflammatory drug indomethacin on cartilage injury and inflammation in experimental OA mice.