Flaveria trinervia (Spreng) C. Mohr is a plant traditionally used in Mexican medicine. In this study, gas chromatography–mass spectrometry (GC–MS) combined with network pharmacology was employed to characterize volatile and semi-volatile metabolites from F. trinervia leaves and to explore their potential system-level mechanisms of action in inflammatory and tumor-related disorders. A dual extraction strategy (hexane/dichloromethane and acetone/chloroform) was applied, followed by GC–MS-based compound identification. Putative molecular targets were predicted using established pharmacological databases, and protein–protein interaction networks were constructed to identify topological features and enriched biological pathways. A total of 11 bioactive compounds were tentatively identified with an identity level of ≥80%, with seven shared between both extracts, including phytol, germacrene D, caryophyllene oxide, pinene isomers, squalene, and 2,2′:5′,2″-terthiophene, metabolites previously reported to exhibit antioxidant, anti-inflammatory, and cytotoxic activities. Network topology analysis identified ESR1, RXRA/B/G, NCOA2, and CYP19A1 as central nodes, reflecting convergence on signaling axes involved in apoptosis, cell proliferation, immune modulation, and transcriptional regulation pathways. Functional enrichment analysis revealed significant associations with KEGG pathways related to immune modulation, neuroendocrine regulation, and cancer-associated pathways. Collectively, these findings suggest a multitarget biological and multipathway pharmacological profile for F. trinervia, consistent with previously reported biological activities. The concordance between in silico predictions and existing experimental evidence strengthens the pharmacological relevance of the identified metabolites and supports their prioritization for further experimental validation, including mechanistic and pharmacokinetic studies, in metabolic, immune, neurological, and cancer-related contexts.

Adiposity-based chronic disease (ABCD) encompasses the health consequences of excess or dysfunctional adipose tissue. Selected phytochemicals have been investigated as potential adjuncts, but experimental pathway activity does not establish clinical benefit. This narrative review examines quercetin, chlorogenic acids, epigallocatechin-3-gallate (EGCG), and berberine, with other interventions providing context. The evidence was supplemented by targeted PubMed searches through 27 October 2026 and appraised according to experimental model, formulation, exposure, clinical relevance, and safety. Published pooled body-weight differences were −0.35 kg (95% confidence interval, −2.03 to 1.33) for quercetin, −1.30 kg (−2.07 to −0.52) for selected green-coffee/chlorogenic-acid interventions, −0.74 kg (−0.97 to −0.51) for green-tea preparations, and −0.88 kg (−1.36 to −0.39) for berberine. These source-specific estimates are not head-to-head comparisons. A small crossover trial of quercetin reported reduced hepatic fat, whereas a six-month berberine trial found no significant benefit for visceral or hepatic fat. Coffee and green-tea findings do not isolate the effects of chlorogenic acid or EGCG. Most mechanistic evidence remains preclinical, and differences in chemical composition, circulating metabolites, administration, and outcome selection limit translation. The human-evidence-based selection also underrepresents less-studied phytochemicals; for the evaluated interventions, sustained adiposity reduction and patient-relevant benefit remain insufficiently established. Their potential role in comprehensive ABCD care requires product-specific assessment of efficacy, exposure, adverse effects, and interactions.

Background: Bone metastasis is a frequent and debilitating complication of advanced cancer, particularly in breast and prostate cancer, and is driven by complex interactions among tumor cells, bone-resident cells, immune populations, vascular components, and the extracellular matrix. Within this specialized microenvironment, proteoglycans have emerged as key molecular regulators of tumor–bone crosstalk, matrix remodeling, metastatic niche formation, dormancy, and therapeutic resistance. Methods: We conducted a narrative review using targeted searches of PubMed and Google Scholar for studies published through 31 May 2026. Search terms included combinations of proteoglycan- and glycosaminoglycan-related concepts, including “proteoglycans,” “glycosaminoglycans,” “heparan sulfate proteoglycans,” “hyaluronan,” “heparanase,” “syndecans,” “glypicans,” “perlecan/HSPG2,” “versican,” and “decorin,” with disease- and process-related terms such as “bone metastasis,” “extracellular matrix,” “tumor–bone crosstalk,” “breast cancer,” “prostate cancer,” “metastatic niche,” “osteolytic metastasis,” “osteoblastic metastasis,” “dormancy,” “reactivation,” “immune regulation,” and “therapy resistance.” Original studies, reviews, and translational reports were selected according to their relevance to cell-surface, pericellular, and extracellular proteoglycans in bone metastatic progression. Results: Proteoglycans and associated GAG/ECM axes are implicated in multiple processes involved in skeletal metastasis, including growth factor availability, extracellular matrix organization, osteolytic and osteoblastic niche formation, angiogenesis, immune evasion, metastatic dormancy, reactivation, and therapy resistance. These functions are highly context-dependent and are influenced by proteoglycan localization, core protein structure, glycosaminoglycan composition, sulfation patterns, proteolytic processing, and cellular source. Conclusions: Proteoglycans represent critical molecular nodes in the bone metastatic microenvironment and hold potential as biomarkers, therapeutic targets, and tools for stratifying metastatic niche heterogeneity. Their clinical translation will require validation in human bone metastasis samples, improved models that reproduce the mineralized and immune-rich bone niche, and a clearer distinction between causal mechanisms and correlative associations. Future studies should integrate matrisome profiling, spatial proteomics, single-cell and spatial transcriptomics, glycosaminoglycan omics, degradomics, and three-dimensional bone niche models to define actionable proteoglycan-dependent mechanisms and improve therapeutic targeting of metastatic bone disease.