The Regnase family comprises RNA-binding endoribonucleases that control immune responses by regulating the stability of inflammation-associated messenger RNA (mRNA). Evidence is most extensive for Regnase-1, whereas the other family members differ in cellular distribution, RNA substrates, and contributions across disease stages. Regnase activity is shaped by the timing of ribonuclease inactivation and recovery, the target-RNA repertoire of each cell type, and intercellular communication. Transient loss of activity after stimulation permits immune effector programs to begin, but failure to restore activity can prolong inflammation. Conversely, persistently high activity in selected T-cell populations or during tissue repair may also disturb homeostasis. Regnase-associated pathology is therefore better understood as a mismatch between RNA decay and the requirements of a particular cell and disease stage than as a uniform increase or decrease in expression. Oligonucleotides targeting autoregulatory stem-loops in the Regnase-1 3' untranslated region, together with local protein or gene augmentation, have provided preclinical proof of concept. Other delivery and protein-regulation platforms remain exploratory. Progress toward therapy will require temporally resolved human samples and direct measurements of protein state, RNA binding, and target decay to define interventions that are cell selective, reversible, and confined to an appropriate disease window.

Melatonin (N-acetyl-5-methoxytryptamine) is a pleiotropic indoleamine involved in diverse physiological and cellular processes and has consequently been investigated in numerous disease models. This molecule is primarily produced in the pineal gland and is well-known for its diverse functions including antitumor, immunomodulatory, antioxidant, antihypertensive, and sedative effects. It is also involved in the regulation of body weight, gastrointestinal function, reproduction, thermoregulation, and cardioprotection. Melatonin exerts its protective effects by modulating various molecular pathways. Among the signaling pathways implicated in these effects, the sirtuin-1 (SIRT1) pathway has received considerable attention. SIRT1 is a well-studied member of the mammalian sirtuin family that functions as a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase. SIRT1 shuttles between the cytoplasm and the nucleus, where it deacetylates histones and other proteins. This activity impacts various cellular functions such as cell survival, metabolism, growth, aging, and stress resistance. Available evidence suggests that melatonin may modulate SIRT1 activity and thereby influence processes involved in inflammation, oxidative stress, apoptosis, and autophagy in various pathological conditions. However, evidence regarding the role of SIRT1 in the effects of melatonin remains limited In this review, we examine the pharmacological effects of melatonin across several disease models, with particular emphasis on the potential involvement of SIRT1 signaling.

Pulmonary fibrosis (PF) is a progressive interstitial lung disease driven by excessive fibroblast activation and extracellular matrix (ECM) deposition, for which pirfenidone and nintedanib slow but do not halt disease progression. Extracellular vesicles (EVs)-lipid bilayer-enclosed nanoparticles that shuttle microRNAs (miRNAs), proteins, and lipids between cells-are increasingly recognized as important mediators and potential modulators of fibrotic remodeling. On the pathogenic side, epithelial- and immune-cell-derived EVs can deliver pro-fibrotic miRNAs (e.g., miR-494-3p) that regulate transforming growth factor beta (TGF-β)/Smad and Wnt/β-catenin signaling, promoting fibroblast-to-myofibroblast transition and ECM accumulation. Conversely, selected mesenchymal stem cell-derived EV (MSC-EV) preparations have demonstrated anti-fibrotic effects in preclinical models through modulation of TGF-β/Smad signaling, M2 macrophage polarization, mitochondrial function, and epithelial-mesenchymal transition; a phase I clinical study has provided initial safety evidence for nebulized administration, although therapeutic efficacy in PF has not yet been established. Beyond MSC-EVs, plant-derived and milk-derived EVs have emerged as potential delivery platforms, although their applications remain largely preclinical. Meanwhile, EVs isolated from plasma, bronchoalveolar lavage fluid, sputum, and urine carry disease-associated molecular signatures that may serve as candidate biomarkers for PF detection or monitoring, but require further clinical validation. This review synthesizes recent evidence on the dual roles of EVs in PF pathogenesis and therapy, evaluates their potential diagnostic utility, and discusses translational hurdles-including cargo standardization, targeted delivery, and scalable manufacturing-that must be overcome for clinical adoption.

Ovarian cancer remains one of the most lethal gynecological malignancies worldwide due to late-stage diagnosis, poor prognosis, and frequent chemoresistance. The limited sensitivity and specificity of current diagnostic approaches, particularly for early-stage disease, highlight the urgent need for improved biomarkers and diagnostic strategies. Nowadays, ovarian cancer diagnostics are based mainly on the established biomarkers CA125 and HE4, which in some countries most commonly combined in the Risk of Ovarian Malignancy Algorithm (ROMA). Despite their widespread clinical use, these biomarkers are of limited specificity and sensitivity, particularly in early-stage disease, underscoring the need for more efficient screening and diagnostic approaches. This review summarizes current evidence on the molecular mechanisms linking oxidative stress, inflammation, and platelet activation with ovarian cancer progression and discusses the diagnostic and prognostic potential of related biomarkers. Oxidative stress and inflammation contribute to dysregulated signaling pathways and tumor progression, providing a mechanistic basis for the identification of novel biomarkers. Increasing evidence indicates that platelet activation contributes to tumor growth, angiogenesis, and metastasis. This justifies the strategy of exploring platelet-derived mediators, including thromboxane B2 and other eicosanoids, as potential biomarkers of ovarian cancer. Overall, current evidence indicates that oxidative stress-, inflammation-, and platelet-associated molecular pathways represent promising sources of novel biomarkers and potential therapeutic targets in ovarian cancer.