How does the collective interaction of many individual cells create a perfectly formed organism? This question is the focus of a new study.

As bones weaken with age, the culprits may be the aging cells within. A new review uncovers how cellular changes—like senescence, inflammation, and loss of regenerative capacity—disrupt the delicate balance of bone formation and breakdown. By mapping these age-related mechanisms across multiple skeletal diseases, the study offers a clearer picture of how bones decline over time, and where potential therapies might intervene to slow or even reverse the process.

New research from the University of the Witwatersrand in Johannesburg, South Africa (Wits University), has shown that heavy metals such as lead, arsenic, cadmium and mercury accumulate in the scales of Black Mambas (Dendroaspis polylepis).

The study, conducted on snakes captured in Durban in KwaZulu-Natal and published in Environmental Pollution, was the first of its kind to examine heavy metal accumulation in an African snake species. The results mean that researchers can use scale clippings from these snakes to accurately measure spatial patterns of environmental pollution levels, without harming the snakes. 

SRPX2 is a chondroitin sulfate proteoglycan (CSPG) exhibiting significant N-glycosylation, which influences its conformation, interactions, and functions, as evidenced by the enhanced glycosylation and functional impact of the N327S mutation. It plays versatile roles in multiple diseases. SRPX2 promotes cancer progression (e.g., gastric, pancreatic, thyroid, glioblastoma) by enhancing proliferation, migration, invasion, and chemoresistance via pathways like TGF-β, PI3K/AKT, Wnt/β-catenin, and FAK/SRC/ERK, correlating with poor prognosis. SRPX2 also plays critical roles in neurodevelopment; mutations are linked to language disorders, autism spectrum disorder (ASD), and potentially Rolandic epilepsy (though evidence is complex and may involve interactions like GRIN2A). SRPX2, a protein characterized by sushi repeat domains, plays a crucial role in synaptogenesis and modulates complement-mediated synaptic pruning processes. Additionally, SRPX2 contributes to idiopathic pulmonary fibrosis via TGF-β signaling, angiogenesis via μPAR/integrin signaling, myocardial infarction protection by inhibiting PI3K/AKT/mTOR, and other conditions. Its context-dependent roles, e.g., pro-fibrotic in lungs vs. protective in heart, and involvement in key signaling pathways highlight its potential as a therapeutic target, though challenges like inhibitor specificity remain.