How complement pathways generate C3b, anaphylatoxins and C5b–9; why endothelial injury is tissue-specific and what positive, negative and retracted clinical findings show.
Two TNF forms, TNFR1 ubiquitin platforms, caspase-8 and MLKL, TNFR2 signaling and the limits of translating cellular mechanisms into clinical therapy.
Dendritic cells: TLRs, MHC-I/MHC-II processing, cross-presentation, metabolism and tolerance. ZOE-50, IMPACT and the negative ACCESS result.
Four CD4+ T-cell programs: receptors, transcription, epigenetics and metabolism, clinical trials, and limits of supplement claims.
PAD4, NOX2, myeloperoxidase and elastase enzymology; NETs in thrombosis and autoimmunity, chromatin clearance and negative DNase trials.
How IL-6 receptors, ADAM10/17 proteolysis, and JAK–STAT3 shape tissue responses, what olamkicept trials found, and why selectivity has limits.
How AKBA modulates lipoxygenases, why exposure limits mechanistic translation, and what positive and negative Boswellia trials show.
NLRP3 assembly, priming, K⁺ efflux, IL-1β/IL-18 maturation, and clinical evidence are considered separately. Inflammaging is not one sensor, and IL-1β blockade is not direct NLRP3 inhibition.
UDCA stereochemistry, bile salt hydrophilicity, AE2/CFTR bicarbonate secretion, mitochondrial stress and transport. Why PBC benefit, PSC high-dose harm and pregnancy outcomes must be assessed separately.
How small-intestinal fungal growth is investigated, what SAP, candidalysin and Candida biofilms can explain, and why experimental mechanisms do not establish a universal treatment protocol.
Electron transfer across eNOS monomers, BH4/BH2 and DHFR, protein redox modifications and NO–cGMP. Arterial mechanics, FMD/cfPWV, biomarkers and limits of clinical recoupling.
11β-HSD1, H6PD, lipid flux and tissue cortisol action: cellular, animal and human evidence, diagnostic limitations and why supplements do not establish a treatment protocol.
Bile-acid synthesis and conjugation, BSH/bai, enterohepatic transport, FXR–FGF19 and TGR5. Lipids, GLP-1, thermogenesis, MASH trials and evidence limits.
HS, HA, syndecan and glypican architecture; shear signaling, eNOS, SOD3, and antithrombin. Revised Starling forces, rheology, renal and brain barriers, indirect PBR and biomarkers, and positive and negative repair trials.
D1/D2/D3 selenium chemistry, ring-specific reactions, compartments, transport and receptors. Reversible D2 ubiquitination, NTIS, selenium trials, Thr92Ala and the limits of laboratory conversion indices without universal treatment protocols.
