The new perspective of using waste biomass to cultivate mushrooms as a source of protein for human nutrition, in line with the circular economy principles, is receiving increasing attention in the scientific community and represents great wealth in terms of environmental sustainability. Pleurotus eryngii is a mushroom also known as cardunculus mushroom due to its ability to grow on this plant. This study explores the potential intrinsic properties of cardunculus (for example, the presence of inulin in the roots) as raw material for the growth of cardunculus mushrooms, and the influence on heteroglycan content and nutrition parameters of the fruiting bodies. Both mycelium and fruiting bodies were used to determine the heteroglycan content in the presence of inulin or cardunculus roots rich in inulin. To produce heteroglycans from P. eryngii in greater quantities and shorter times without having to wait for the formation of the fruiting bodies, the mycelium could be used. The results showed that the presence of cardunculus biomass positively influences the heteroglycan content of P. eryngii. In terms of nutritional parameters, higher contents of polyphenols, flavonoids, anthocyanins, and antioxidant activity were detected in P. eryngii grown on the cardunculus stem and root substrate. In conclusion, recycling cardunculus biomass to generate growth blocks for edible mushrooms is a winning choice due to the opportunity to use this biomass waste, which is gaining more and more attention due to the increase in cultivated areas and the use of fruiting bodies of P. eryngii as a functional food and source of molecules with potential biological activities.

Hematological malignancies are among the top five most frequent forms of cancer in developed countries worldwide. Although the new therapeutic approaches have improved the quality and the life expectancy of patients, the high rate of recurrence and drug resistance are the main issues for counteracting blood disorders. Chemotherapy-resistant leukemic clones activate molecular processes for biological survival, preventing the activation of regulated cell death pathways, leading to cancer progression. In the past decade, leukemia research has predominantly centered around modulating the well-established processes of apoptosis (type I cell death) and autophagy (type II cell death). However, the development of therapy resistance and the adaptive nature of leukemic clones have rendered targeting these cell death pathways ineffective. The identification of novel cell death mechanisms, as categorized by the Nomenclature Committee on Cell Death (NCCD), has provided researchers with new tools to overcome survival mechanisms and activate alternative molecular pathways. This review aims to synthesize information on these recently discovered RCD mechanisms in the major types of leukemia, providing researchers with a comprehensive overview of cell death and its modulation.

Background: Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and are strongly influenced by dietary habits. Beyond caloric intake, nutrients act as molecular signals that regulate cardiac metabolism, mitochondrial function, inflammation, and epigenetic remodeling. Objectives: This review aims to synthesize current evidence on how dietary patterns and specific nutritional interventions regulate cardiac metabolism and function through interconnected molecular and epigenetic mechanisms, highlighting their relevance for cardiovascular disease prevention. Methods: A narrative review of the literature was conducted using PubMed, Scopus, and Web of Science, focusing on studies published between 2006 and 2025. Experimental, translational, and clinical studies addressing diet-induced modulation of cardiac metabolic pathways, oxidative and inflammatory signaling, epigenetic regulation, and gut microbiota-derived metabolites were included. Results: The analyzed literature consistently shows that unbalanced diets rich in saturated fats and refined carbohydrates impair cardiac metabolic flexibility by disrupting key nutrient-sensing pathways, including AMP-activated protein kinase (AMPK), proliferator-activated receptor alpha (PPARα), mammalian target of rapamycin (mTOR), and sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (SIRT1/PGC-1α), leading to mitochondrial dysfunction, oxidative stress, chronic inflammation, and maladaptive remodeling. In contrast, cardioprotective dietary patterns, such as caloric restriction (CR), intermittent fasting (IF), and Mediterranean and plant-based diets, enhance mitochondrial efficiency, redox balance, and metabolic adaptability. These effects are mediated by coordinated activation of AMPK-SIRT1 signaling, suppression of mTOR over-activation, modulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2) pathways, and favorable epigenetic remodeling involving DNA methylation, histone modifications, and non-coding RNAs. Emerging evidence also highlights the central role of gut microbiota-derived metabolites, particularly short-chain fatty acids, in linking diet to epigenetic and metabolic regulation of cardiac function. Conclusions: Diet quality emerges as a key determinant of cardiac metabolic health, acting through integrated molecular, epigenetic, and microbiota-mediated mechanisms. Targeted nutritional strategies can induce long-lasting cardioprotective metabolic and epigenetic adaptations, supporting the concept of diet as a modifiable molecular intervention. These findings provide a mechanistic rationale for integrating personalized nutrition into cardiovascular prevention and precision cardiology, complementing standard pharmacological therapies.

Ferroptosis, an iron-dependent form of regulated cell death marked by lipid peroxidation, is critically implicated in the pathology of acute myeloid leukemia (AML). The dysregulation of iron metabolism and ferroptotic regulators, such as GPX4, the cystine/glutamate antiporter System Xc⁻, and several iron homeostasis proteins, contributes to leukemic cell survival and therapy resistance. These disruptions not only facilitate the survival and proliferation of leukemic cells but also enable them to evade traditional apoptotic pathways, thereby increasing resistance to standard therapeutic interventions. Recent studies have focused on identifying specific targets within the ferroptosis pathway that are aberrantly expressed in AML, highlighting potential vulnerabilities that can be exploited for therapeutic benefit. Promising compounds such as Erastin and RSL3 have emerged as effective inducers of ferroptosis in AML cells, demonstrating the capacity to circumvent resistance mechanisms. These agents function by inhibiting GPX4 and disrupting cystine uptake, which culminates in enhanced lipid peroxidation and cell death. This chapter explores the therapeutic potential of targeting ferroptosis in AML, with a particular focus on modulating iron metabolism and key regulatory pathways. By exploiting the vulnerabilities in ferroptotic processes, these strategies offer a novel approach to enhancing therapeutic efficacy and addressing the critical challenge of drug resistance in AML.