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Item type:Publication, T he interplay between osteoarthritis and cardiovascular disease: shared pathophysiological mechanisms(2026)The relationship between osteoarthritis (OA) and cardiovascular disease (CVD) is complex. Epidemiologically, both OA and CVD have displayed rising trends in the last decades, largely attributed to consistent increases in the prevalence of overlapping risk factors. Furthermore, subjects with OA appear to have a greater cardiovascular risk. As a result, these conditions are associated with a significant burden for public health systems. Both OA and CVD have traditionally been studied as distinct conditions, yet growing epidemiological and molecular evidence suggests these two highly prevalent chronic diseases are linked not merely by shared risk factors such as aging, obe-sity, and sedentary lifestyle, but also by deeply interconnected biological mechanisms. In ensemble, a plethora of pathophysiologic phenomena, such as chronic inflammation, oxidative stress, adipokine dysregulation, endothelial dysfunction, and extracellular matrix remodeling form a complex and overlapping network of processes that can jointly drive both articular degradation and vascular injury. Bridging the gap between musculoskeletal and cardiovascular research offers the promise of innovative therapies and integrated care strategies that can improve both mobility and longevity for millions of patients worldwide by improving clinical outcomes of both OA and CVD. In this narrative review, we revise the pathophysiological interconnections between OA and CVD. © 2026, Venezuelan Society of Pharmacology and Clinical and Therapeutic Pharmacology. All rights reserved.4 - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Endometriosis as a Systemic and Complex Disease: Toward Phenotype-Based Classification and Personalized Therapy(2026); ;Emilia Jiménez-Flores ;Martha Montalvan ;Raquel HorowitzValeria AraujoEndometriosis is traditionally conceptualized as a pelvic lesion–centered disease; however, mounting evidence indicates it is a chronic, systemic, and multifactorial inflammatory disorder. This review examines the molecular dialog between ectopic endometrial tissue, the immune system, and peripheral organs, highlighting mechanisms that underlie disease chronicity, symptom variability, and therapeutic resistance. Ectopic endometrium exhibits distinct transcriptomic and epigenetic signatures, disrupted hormonal signaling, and a pro-inflammatory microenvironment characterized by inflammatory mediators, prostaglandins, and matrix metalloproteinases. Immune-endometrial crosstalk fosters immune evasion through altered cytokine profiles, extracellular vesicles, immune checkpoint molecules, and immunomodulatory microRNAs, enabling lesion persistence. Beyond the pelvis, systemic low-grade inflammation, circulating cytokines, and microRNAs reflect a molecular spillover that contributes to chronic pain, fatigue, hypothalamic–pituitary–adrenal axis dysregulation, and emerging gut–endometrium interactions. Furthermore, circulating biomarkers—including microRNAs, lncRNAs, extracellular vesicles, and proteomic signatures—offer potential for early diagnosis, patient stratification, and monitoring of therapeutic responses. Conventional hormonal therapies demonstrate limited efficacy, whereas novel molecular targets and delivery systems, including angiogenesis inhibitors, immune modulators, epigenetic regulators, and nanotherapeutics, show promise for precision intervention. A systems medicine framework, integrating multi-omics analyses and network-based approaches, supports reconceptualizing endometriosis as a systemic inflammatory condition with gynecologic manifestations. This perspective emphasizes the need for interdisciplinary collaboration to advance diagnostics, therapeutics, and individualized patient care, ultimately moving beyond a lesion-centered paradigm toward a molecularly informed, holistic understanding of endometriosis.11
