Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. While timely reperfusion therapies such as percutaneous coronary intervention (PCI) and thrombolysis are essential for salvaging ischemic myocardium, they can paradoxically exacerbate tissue injury through a process known as myocardial infarction reperfusion injury (MIRI). MIRI can contribute to up to 50% of the final infarct size, significantly diminishing the benefits of revascularization and leading to worsened cardiac outcomes. The pathophysiology of MIRI involves complex, interrelated mechanisms including oxidative stress, calcium overload, mitochondrial dysfunction, inflammatory responses, apoptosis, and dysregulated autophagy. Post-reperfusion recovery is further complicated by structural and functional abnormalities such as microvascular obstruction, endothelial dysfunction, and myocardial stunning. Clinically, distinguishing reperfusion injury from ischemic damage is challenging and often requires the use of sensitive biomarkers, such as cardiac troponins, alongside advanced imaging modalities. Although a range of pharmacological (e.g., antioxidants, calcium channel blockers, mitochondrial stabilizers, anti-inflammatory agents) and non-pharmacological (e.g., hypothermia, gene therapy, stem cell-based therapies) interventions have shown promise in preclinical studies, their clinical translation remains limited. This is largely due to the multifactorial and dynamic nature of MIRI. In this context, network pharmacology offers a systems-level approach to understanding the complex biological interactions involved in MIRI, facilitating the identification of multi-target therapeutic strategies. Integrating network pharmacology with omics technologies and precision medicine holds potential for advancing cardioprotective therapies. This review provides a comprehensive analysis of the molecular mechanisms underlying MIRI, examines the current clinical challenges, and explores emerging therapeutic strategies. Emphasis is placed on bridging the translational gap through validated, multi-target approaches and large-scale, multicenter clinical trials. Ultimately, this work aims to support the development of innovative and effective interventions for improving outcomes in patients with myocardial infarction.

Breast cancer is associated mostly with women; however, breast cancer also appears in men, which dictates the need to know about gender-specific differences in the pathology and treatment. Male breast cancer constitutes less than 1 % of all cases and is usually diagnosed when the patient is older, with bigger tumors and at later stages than breast cancer in women. The most widespread subtype in both genders is invasive ductal carcinoma. The effect of hormone receptor positivity is very prominent in the treatment of men, and the risk factors include the BRCA2 mutations and the hormonal imbalance. The management approach, such as surgery, chemotherapy, radiotherapy, and hormonal therapy, is like that of women, and it may vary in treatment effectiveness because of hormonal and biological differences. The prognostic data in males are scarce, with generally worse outcomes, most likely because of delayed diagnosis and low rates of clinical trial representation. Men with breast cancer also face special psychosocial obstacles with regard to stigma and support. The use of artificial intelligence (AI) and machine learning are emerging options that have the potential to improve detectability and personalized treatment in both genders. The current review draws similarities between breast cancer in males and females to promote gender-specific interventions and better outcomes.

Urolithiasis is a complex and multifactorial disease with rising global prevalence. Traditional management strategies primarily focus on symptom relief and surgical intervention. However, with advances in genomics, metabolomics, and imaging technologies, precision medicine is reshaping the diagnostic and therapeutic landscape of kidney stone diseases. This review explored the integration of genetic screening, individualized metabolic evaluation, and risk stratification to enable tailored treatment plans. We discuss the current and emerging approaches that align with the principles of precision medicine, including the identification of monogenic and polygenic risk factors, advanced imaging for stone composition, and targeted lifestyle or pharmacological interventions. These developments herald a paradigm shift in urolithiasis care, moving beyond reactive treatment toward proactive, patient-specific management.

Liver disease poses potential therapeutic challenges, as ongoing hepatic injury is correlated with oxidative stress, inflammation, mitochondrial dysfunction, fibrosis, and impaired hepatocellular function. There are many medicinal plants and their bioactive ingredients with hepatoprotective, antioxidant, and anti-inflammatory properties, but their effectiveness is restricted by problems with water solubility, bioavailability, instability, rapid metabolism, and hepatic delivery. To address this issue, the use of nanocarriers for the delivery of herbal bioactives has become a promising approach to enhance their therapeutic potential. This review focuses on a targeted introduction of the herbal nanocarrier-based treatment approach for liver diseases and the correlation between the various properties of the nanocarrier and the enhancement effect of the plant-derived compounds’ delivery in the liver. Important nanocarrier-based systems such as liposomes, phytosomes, niosomes, solid lipid nanoparticles, nanostructured lipid carriers, polymeric nanoparticles, dendrimers, and other emerging systems are mentioned in relation to their structural features, drug-loading capacity, stability, controlled-release features, bioavailability, and hepatic targeting possibilities. It also highlights some of the herbal bioactives that have been attached to nanocarriers and their uses in hepatotoxicity, fatty liver syndrome, fibrosis, inflammation, and liver cancer. Mainly the nanocarriers help increase the solubility of bioactive molecules, prevent their degradation, extend systemic action, improve their accumulation in the liver, and increase their efficacy in treatment relative to classical herbal formulations. Finally, current state-of-the-art limitations, formulation challenges, safety and standardization aspects, and future possibilities for clinical translation in the context of herbal nanocarrier systems are presented.

Short-chain fatty acids (SCFAs), primarily acetate, propionate, and butyrate, are key microbial metabolites generated through the fermentation of indigestible carbohydrates by gut bacteria. Beyond their local actions in the intestinal environment, these metabolites exert far-reaching systemic effects, particularly in shaping neuroimmune communication along the gut–brain axis. Their interaction with free fatty acid receptor 2 (FFAR2), expressed on intestinal epithelial cells, peripheral immune populations, and microglia, has emerged as a central mechanism linking gut microbial activity to neuroinflammatory regulation. Disrupted FFAR2 signalling and altered SCFA production are now implicated in the pathogenesis of key neuroinflammatory and neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. In this narrative review, we synthesize current evidence suggesting that SCFAs can mediate microglial development, cytokine cross-linking, and barrier stability, as well as neuronal-glial communication via FFAR2-mediated and receptor-independent mechanisms, including HDAC inhibition. Importantly, current evidence supports three partially overlapping mechanistic frameworks: (i) direct receptor-dependent signalling, including potential FFAR2-mediated effects on microglia, although such expression and functional relevance in adult microglia remain debated; (ii) receptor-independent intracellular mechanisms, particularly histone deacetylase (HDAC) inhibition and metabolic reprogramming; and (iii) indirect peripheral immune and gut–brain regulatory pathways, involving modulation of systemic cytokine milieus, barrier integrity, and immune cell trafficking, which appear to be more consistently supported in adult in vivo models. Experimental research shows that restoring SCFA supply or activating FFAR2 can suppress neuroinflammation, increase the clearance of pathological proteins by proteases, and promote neuronal survival. Available strategies to increase endogenous SCFA production include dietary fiber consumption, prebiotics, and customized SCFA formulations, and novel synthetic FFAR2 agonists offer a pharmacological approach to targeted therapy. Nonetheless, there remains a significant degree of variability in dosing, route of delivery, bioavailability, and interindividual microbiota profiles, which restricts clinical translation. Combined, the existing knowledge base places the SCFA-FFAR2 axis as an encouraging therapeutic agent regarding altering neuroimmune responses and creating new approaches to the control of neuroinflammatory and neurodegenerative diseases.