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Janus kinase inhibitors (JAKi) including tofacitinib and baricitinib modulate SLE pathogenesis via JAK/STAT pathway inhibition, with preclinical evidence revealing tofacitinibs dual capacity to reduce NET burden and restore endothelial homeostasis in MRL/lpr models (148150)

Potential pathways include improvements in endothelial function, reductions in blood pressure, anti-inflammatory effects, and direct myocardial protection, all of which have been described with GLP-1RA therapy independent of weight change [12,13,14]

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This review redefines the pathophysiology of severe acute pancreatitis-associated multiple organ dysfunction (SAP-MODS) by exploring the glycocalyxs central mechanistic role and proposes stabilizing glycocalyx structure as a potential strategy to prevent microcirculatory failure

Curcumin prevents Cr(VI)-induced renal oxidant damage by a mitochondrial pathway

& Gresser, U