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In particular, when homocysteine attached to a protein called syntaxin 17, it blocked the protein from performing its role of transporting and digesting fat (known as autophagy, an essential cellular process by which cells remove malformed proteins or damaged organelles) in fatty acid metabolism, mitochondrial turnover, and inflammation prevention

This interaction between exosomes and hBMSCs highlights the potential of targeting EV-mediated signaling in GBM therapy

The researchers used both in vitro cell culture (HaCaT keratinocytes and primary human dermal papilla cells) and in vivo mouse models

It's supposedly the homocysteine coming out of the system