Myocardial ischemia/reperfusion (I/R) injury causes cardiomyocyte death and exacerbates inflammation. Emerging evidence implicates extracellular RNA (eRNA) and tumor necrosis factor-α (TNF-α) as key mediators. We hypothesize that eRNA released from ischemic cardiomyocytes amplifies I/R injury via TNF-α/TNF-receptor-1 (TNF-R1) signaling, and that hydrolysis of eRNA by RNase1 can attenuate I/R injury by disrupting this pathway. Here, we investigated the mechanistic role of eRNA and its interplay with TNF-α signaling in cardiac I/R injury, and evaluated the therapeutic potential of RNase1 and cyclosporine-A (CsA). In ST-segment elevation myocardial infarction patients, plasma eRNA levels were significantly elevated 2 h post-percutaneous coronary intervention (PCI), correlating positively with Creatine Kinase (CK). In murine I/R and hypoxia/reoxygenation models, eRNA released from stressed cardiomyocytes acted as a damage-associated molecular pattern, triggering TNF-α shedding via TACE/ADAM17 and activating TNF-R1-mediated inflammation, mPTP opening, and cell death. Genetic deletion of TNF-α or TNF-R1 abrogated eRNA-induced cytotoxicity, while TNF-receptor- 2 (TNF-R2) deficiency exacerbated injury. Pharmacological inhibition of TACE with TAPI suppressed TNF-α release and preserved cell viability. RNase1 effectively degraded eRNA, blocking upstream pro-inflammatory signaling, whereas CsA preserved mitochondrial integrity by preventing mPTP opening. Notably, RNase1 and CsA showed synergistic protection in vivo when administered at reperfusion, significantly reducing myocardial infarct size. These findings identify eRNA as both a biomarker and pathogenic mediator of myocardial I/R injury, and support a dual-targeted strategy using RNase1 and CsA to interrupt the TNF-α/TNF-R1-driven inflammatory and mitochondrial death pathways. Targeting both upstream inflammatory and downstream mitochondrial mechanisms represents a promising cardioprotective intervention for acute myocardial infarction.

Biofilms are structured microbial communities that adhere to biotic and abiotic surfaces embedded in an autonomous extracellular matrix. These structures contribute to persistent infections, especially in patients with indwelling medical devices, due to their resistance to antimicrobial agents; they have evolved to evade host immune responses. Despite advances in antimicrobial therapies, biofilm-associated infections remain a major challenge in clinical infectious diseases. This perspective explores the underlying mechanisms of biofilm resilience and immune evasion, emphasizing the limitations of conventional treatments and the need to develop pre-emptive measures that focus on preventing biofilm formation rather than implementing a treatment. This work discusses emerging strategies, such as quorum-sensing inhibition, hormonal modulation, matrix-degrading enzymes, anti-adhesive surface modifications, and nanotechnology-based drug delivery, that offer promising avenues to disrupt biofilm formation and maturation. Also offers a shift from the paradigm, looking into proactive prevention rather than treatment, emphasizing clinical translation, scalability, and biocompatibility. Embedding these strategies into routine care could significantly reduce healthcare-associated infections, improve patient outcomes, and mitigate the development of antimicrobial resistance. Our analysis highlights biofilm prevention as a critical frontier in the future of infectious disease management.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, primarily driven by chronic inflammation from viral hepatitis, metabolic dysfunction, alcohol-induced liver disease, and cirrhosis. Conventional therapies often fail in advanced stages, highlighting the need for mechanism-based, precision-guided interventions. Plant-derived secondary metabolites represent a promising class of bioactive compounds with structural diversity, multitarget activity, anti-inflammatory effects, and favorable toxicity profiles. This review follows a semi-systematic narrative that synthesizes preclinical and experimental evidence on the anti-inflammatory and anticancer properties of key phytochemicals, including epigallocatechin-3-gallate, galangin, resveratrol, quercetin, curcumin, berberine, genistein, and thymoquinone. These compounds consistently modulate critical inflammation-driven signaling pathways, PI3K/AKT/mTOR, NF-κB, JAK/STAT, Wnt/β-catenin, and MAPK, resulting in apoptosis induction, cell cycle arrest, inhibition of angiogenesis, and reduced invasion and metastasis in multiple HCC models. Despite strong preclinical evidence, clinical translation remains limited by variable bioavailability, incomplete safety data, and insufficient human studies. A staged development strategy is recommended: standardized formulations, Good Laboratory Practice-compliant pharmacokinetic/toxicology studies, validation in patient-derived models, and early-phase, biomarker-guided clinical trials with combination therapy arms. Addressing regulatory, manufacturing, and quality control considerations will be essential for advancing these compounds as adjuvant or complementary agents in precision HCC therapy.

El cambio climático se ha consolidado como un determinante crítico en la dinámica epidemiológica global, afectando directamente la incidencia, distribución y severidad de las enfermedades infecciosas. Este fenómeno, impulsado por actividades antropogénicas, modifica patrones climáticos, altera ecosistemas y favorece la emergencia de zoonosis al incrementar el contacto entre humanos y reservorios animales. Asimismo, eventos extremos como inundaciones, sequías y huracanes deterioran infraestructuras sanitarias y crean condiciones propicias para la proliferación de vectores como mosquitos, garrapatas y roedores. Estos cambios ambientales, junto con procesos como la deforestación, urbanización no planificada y desplazamientos poblacionales, facilitan la reemergencia de enfermedades transmisibles y su expansión geográfica. Este artículo analiza de forma integral la evidencia científica que vincula el cambio climático con enfermedades como el dengue, el cólera y las infecciones respiratorias, destacando los riesgos crecientes para la salud pública. Se plantea la necesidad urgente de fortalecer sistemas de vigilancia epidemiológica, promover estrategias de mitigación ambiental y fomentar políticas intersectoriales que integren salud, clima y biodiversidad. Concluimos que abordar el cambio climático no solo es una prioridad ambiental, sino también una estrategia esencial para prevenir crisis sanitarias futuras en un contexto de creciente vulnerabilidad global.

Background: Prostate cancer (PCa) arises from complex interactions among host genetics, androgen signaling, and microbial communities. Emerging genomic evidence supports the presence of microbial consortia within prostate tissue, suggesting that microbial genes, metabolites, and host–microbe interactions may contribute to chronic inflammation, oncogenic signaling, and therapeutic resistance. Methods: We conducted a narrative review using targeted searches of PubMed and Google Scholar for studies published between 2020 and 2025, complemented by selected mechanistic reports published in March 2026. Human studies and experimental research providing mechanistic insights into prostate models were prioritized. Due to the heterogeneous methodologies, evidence was synthesized qualitatively, with an emphasis on genomic and signaling perspectives. Results: Low-biomass microbial DNA is consistently detected in prostate tissue. Proteomic analyses of Corpora amylacea suggest a “fossil record” of past infections through sequestered microbial DNA and antimicrobial proteins, potentially priming tissue for long-term carcinogenic processes, although contamination remains a key limitation. Recurrent bacterial and viral signals, including Cutibacterium acnes, Escherichia coli, Pseudomonas, Acinetobacter, human papillomavirus, Epstein–Barr virus, and cytomegalovirus, appear to converge on a restricted set of tumor-relevant pathways, including TLR–NF-κB, MAPK, PI3K/AKT/mTOR, cGAS–STING, and p53/pRb disruption. These interactions may promote cytokine production, oxidative stress, DNA damage, epithelial–mesenchymal transition, extracellular matrix remodeling, immune evasion, and resistance to therapy. The gut–prostate axis further links intestinal dysbiosis and microbial metabolites with systemic IGF-1 signaling and castration resistance. Conclusions: Microbial genomic consortia in the prostate and gut may shape inflammatory, metabolic, and immune networks that influence PCa initiation and progression. However, most available data remain correlative and are limited by low-biomass sampling, contamination risk, and heterogeneous study designs. Future research should prioritize rigorous contamination control, longitudinal and prostate-specific mechanistic studies, and integrated multi-omic approaches to clarify causality and identify actionable microbial targets for prevention, diagnosis, and therapy.