High concentration magnesium inhibits extracellular matrix calcification and protects articular cartilage via Erk/autophagy pathway.

The significant cytopathological changes of osteoarthritis are chondrocyte hypertrophy, proteoglycan loss, extracellular matrix (ECM) calcification, and terminally, the replacement of cartilage by bone. Meanwhile, magnesium ion (Mg ), as the second most abundant divalent cation in the human body, has been proved to inhibit the ECM calcification of hBMSCs (human bone marrow stromal cells), hVSMCs (Human vascular smooth muscle cells), and TDSCs (tendon-derived stem cells) in vitro studies. The ATDC5 cell line, which holds chondrocyte characteristics, was used in this study as an in vitro subject.

Unfractionated Heparin Alleviates Human Lung Endothelial Barrier Dysfunction Induced by High Mobility Group Box 1 Through Regulation of P38-GSK3β-Snail Signaling Pathway.

Background/aims: The high mobility group box 1 (HMGB1) has been regarded as an important inflammatory mediator. Previous studies showed the involvement of HMGB1 protein in the dysfunction of endothelial barrier function during acute lung injury. However, the molecular mechanism remains unclear.

[The role of mitochondrial permeability transition pore in the occurrence of septic myocardial depression].

Sepsis is defined as life-threatening organ dysfunction caused by a dys-regulated host response to infection and septic myocardial depression (SMD) is a common complication. Pathogenesis of SMD is complicated and there is lack of specific treatment. Mitochondrial damage is an important pathological basis of SMD, and mitochondrial permeability transition pore (MPTP) plays an important role in maintaining the normal structure and function of the mitochondria.

Magnesium inhibits the calcification of the extracellular matrix in tendon-derived stem cells via the ATP-P2R and mitochondrial pathways.

Tendon calcification has been widely regarded by researchers to result from the osteogenic differentiation of Tendon-Derived Stem Cells (TDSCs) and ectopic mineralization caused by the calcification of cellular matrix. Recent studies have revealed a correlation between the Mg(2+)/Ca(2+) balance and the degeneration or calcification of tendon tissues. Furthermore, the ATP-P2X/P2Y receptor pathway has been shown to play a decisive role in the process of calcification, with calcium exportation from mitochondria and calcium oscillations potentially representing the cohesive signal produced by this pathway.