Comprehensive analysis of culture conditions governing differentiation of MSCs into articular chondrocytes.

Treatment of osteoarthritic patients requires the development of morphologically and mechanically complex hyaline cartilage at the injury site. A tissue engineering approach toward differentiating mesenchymal stem cells into articular chondrocytes has been developed to overcome the drawbacks of conventional therapeutic and surgical procedures. To imitate the native micro and macro environment of articular chondrocytes, cell culture parameters such as oxygen concentration, mechanical stress, scaffold design, and growth factor signalling cascade regulation must be addressed. This review aims to illuminate the path toward developing tissue engineering approaches, accommodating these various parameters and the role these parameters play in regulating chondrogenesis for better articular cartilage development to treat osteoarthritis effectively.

Osteoarthritis is a common problem where the protective layer of cartilage on the joints wears away. It's difficult to treat with current methods. However, stem cell therapy is a promising alternative that has been researched a lot recently. Stem cells are special cells that can change into different types of tissue, including cartilage. Scientists are trying to figure out how to get these stem cells to grow into cartilage effectively. They are also trying to understand how stem cells find the right place in the body to go and do their job. By modifying the genes of stem cells and using special materials and growth factors, scientists hope to improve the effectiveness of stem cell therapy for osteoarthritis.

Oncogenic metabolic reprogramming in breast cancer: focus on signaling pathways and mitochondrial genes.

Oncogenic metabolic reprogramming impacts the abundance of key metabolites that regulate signaling and epigenetics. Metabolic vulnerability in the cancer cell is evident from the Warburg effect. The research on metabolism in the progression and survival of breast cancer (BC) is under focus. Oncogenic signal activation and loss of tumor suppressor are important regulators of tumor cell metabolism. Several intrinsic and extrinsic factors contribute to metabolic reprogramming. The molecular mechanisms underpinning metabolic reprogramming in BC are extensive and only partially defined. Various signaling pathways involved in the metabolism play a significant role in the modulation of BC. Notably, PI3K/AKT/mTOR pathway, lactate-ERK/STAT3 signaling, loss of the tumor suppressor Ras, Myc, oxidative stress, activation of the cellular hypoxic response and acidosis contribute to different metabolic reprogramming phenotypes linked to enhanced glycolysis. The alterations in mitochondrial genes have also been elaborated upon along with their functional implications. The outcome of these active research areas might contribute to the development of novel therapeutic interventions and the remodeling of known drugs.