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Endometriosis as a Systemic and Complex Disease: Toward Phenotype-Based Classification and Personalized Therapy
(MDPI AG, 2026-01-16)
Daniel Simancas-Racines
;
Emilia Jiménez Flores
;
Martha Montalvan
;
Raquel Horowitz
;
Valeria Araujo
Endometriosis 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.
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The Molecular Mechanisms Underlying Dercum’s Disease: Exploring the Intersection of Obesity, Pain, and Inflammation
(MDPI AG, 2025-11-18)
REYTOR GONZÁLEZ, CLAUDIA MARÍA
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Emilia Jiménez Flores
;
Melannie Toral-Noristz
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Campuzano Donoso Martín
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ROMAN GALEANO, NATHALY MERCEDES
Obesity is increasingly recognized not only as a metabolic disorder, but also as a state of chronic low-grade inflammation that predisposes to systemic complications. Within this context, Dercum’s disease (DD), or adiposis dolorosa, emerges as a rare yet debilitating disorder characterized by painful subcutaneous lipomas, most commonly affecting middle-aged women. Despite its clinical impact, DD remains underdiagnosed and is often misclassified as lipedema, fibromyalgia, or lipomatosis, complicating prevalence estimates and hindering the development of targeted interventions. Current evidence suggests that DD represents a distinctive model of inflammatory obesity, where adipose tissue actively contributes to pain generation rather than serving as a passive fat reservoir. Histological and molecular findings point to adipose tissue dysfunction, immune cell infiltration, and elevated secretion of pro-inflammatory adipokines, signals which appear to fuel systemic low-grade inflammation, perineural immune interactions, and nociceptor sensitization. Peripheral mechanisms further shape the clinical phenotype. While familial clustering suggests possible genetic contributions, no definitive markers have been identified, and the role of obesity-induced epigenetic modifications remains unexplored. Therapeutic strategies remain largely symptomatic, including analgesics, antidepressants, physical rehabilitation, and surgical excision of lipomas, whereas molecularly targeted and diet-based interventions are still experimental. This article discusses the pathophysiology of DD, current treatments, and future perspectives, emphasizing that advancing patient registries, omics-based analyses, and interdisciplinary clinical trials will be crucial to elucidate disease mechanisms and guide novel therapies. Improved understanding of DD may not only enhance patient care, but also provide broader insights into the interplay between obesity, inflammation, and chronic pain.
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Redefining Chemoresistance: Natural Bioactives as Molecular Modulators at the Cancer–Tumor Microenvironment Interface
(MDPI AG, 2025-08-20)
REYTOR GONZÁLEZ, CLAUDIA MARÍA
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Emilia Jiménez Flores
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GONZALEZ CALZADA, NATALI
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SIMANCAS RACINES, DANIEL ALEJANDRO
Therapeutic resistance remains a critical barrier in effective cancer treatment, contributing to disease recurrence, progression, and reduced patient survival. In recent years, natural bioactive compounds have emerged as promising adjuncts in oncology due to their ability to modulate multiple biological processes involved in resistance. This review explores current evidence on the role of natural compounds in influencing cancer cell behavior and their interactions with the tumor microenvironment. By organizing these compounds into chemical families, we provide a structured overview of their potential to enhance the efficacy of standard chemotherapy and reduce resistance-related mechanisms. We also highlight innovative strategies, including combination therapies and advanced drug delivery systems, that aim to improve their clinical applicability. Overall, this work underscores the relevance of integrating natural bioactives into modern cancer therapy and calls for further translational research to bridge preclinical findings with clinical implementation.
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Oesophageal adenocarcinoma, obesity, and cancer: the role of nutrition in prevention and management
(Informa UK Limited, 2025-05-29)
REYTOR GONZÁLEZ, CLAUDIA MARÍA
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SIMANCAS RACINES, DANIEL ALEJANDRO
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Emilia Jiménez Flores
;
Martín Campuzano Donoso
;
Angelo Michele Carella
Oesophageal adenocarcinoma (EAC) is increasingly associated with obesity, metabolic dysfunction, and genetic predispositions. This review explores how nutritional factors interact with these risk elements, emphasizing the potential of dietary strategies in EAC prevention and management. Diets such as the Mediterranean and plant-based patterns may reduce inflammation, oxidative stress, and metabolic imbalance, thereby modulating cancer risk. Nutrient-rich foods–particularly omega-3 fatty acids, cruciferous vegetables, and dietary fibre–offer additional protective effects. Personalized nutrition, tailored to individual genetic and metabolic profiles, is emerging as a promising tool in cancer prevention. Moreover, weight management strategies like caloric restriction and intermittent fasting may contribute to risk reduction. Integrating these approaches into clinical and public health practices could play a critical role in mitigating the underlying drivers of EAC. Further research is needed to strengthen dietary guidelines and advance precision nutrition for high-risk populations.

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