Cells

Natural ingredient-based cosmeceuticals represent an expanding area at the interface of cosmetics; these include polyphenols, phenolic acids, flavonoids, carotenoids, fatty acids, polysaccharides, and essential oil constituents. They have attracted increasing attention because of their antioxidant, anti-inflammatory, antimicrobial, photoprotective, and skin barrier-supporting properties. These compounds may contribute to the prevention of premature skin aging by reducing oxidative stress, modulating inflammatory signaling, inhibiting extracellular matrix degradation, and supporting epidermal homeostasis. In parallel, the emerging concept of microbiome-friendly skincare has created new opportunities for natural ingredients that act as prebiotics, postbiotics, or microbial balance supporting agents. Before clinical translation, cell-based experimental systems employing keratinocytes, dermal fibroblasts, melanocytes, and reconstructed skin models can be used to validate the relevant mechanisms of action at the cellular level. However, the translation of natural bioactivities into effective cosmetic products remains limited by poor chemical stability, low skin penetration, variability in extract composition, formulation incompatibility, and insufficient clinical validation. Advanced formulation technologies, including liposomes, nanoemulsions, solid lipid nanoparticles, hydrogels, and biopolymer-based delivery systems, may improve the stability, bioavailability, and controlled release of natural actives. This review summarizes major classes of plant-derived cosmeceutical ingredients, their mechanisms of action in skin aging, photoaging, barrier repair, and microbiome modulation, and discusses extraction, characterization, formulation, safety, and regulatory considerations. Future development should prioritize standardized phytochemical profiling, mechanism-based efficacy testing, microbiome-aware formulation design, sustainable sourcing, and well-controlled human studies.

Sirtuins (SIRTs) are nicotinic adenine dinucleotide (NAD)⁺-dependent deacetylases regulating critical signaling pathways in prokaryotes and eukaryotes. Recent in vivo and in vitro studies have successfully demonstrated the involvement of SIRT1 in key pathways for the biological function of the cardiovascular system, including cellular metabolism, senescence, oxidative stress, apoptosis and DNA damage. Based on SIRT1 pathophysiology activity, emerging evidence has stimulated a significant evolution in eventually preventing and treating cardiovascular disease (CVDs) by its modulation. SIRT1 is characterized by a protective role against inflammation, vascular aging, arrhythmias and the development of atherosclerotic plaques. Mechanistically, SIRT1 exerts vasculoprotective effects through deacetylation of key transcription factors leading to reduced inflammation, enhanced antioxidant defense, improved endothelial function, and correct vascular remodeling. This review provides a comprehensive overview of SIRT1-controlled molecular signaling pathways in heart pathophysiology, with particular emphasis on atherosclerosis, hypertension, dyslipidemia, atrial fibrillation, cardiac ischemia and ischemic/reperfusion injury. A deeper understanding of the epigenetic mechanisms by which SIRT1 intervenes in signaling pathways responsible for the onset and development of CVDs is important for speeding up the achievement of selective and effective pharmacological modulation of SIRT1 for future applications in the prevention and treatment of CVDs.

Cancer is increasingly understood as a tissue- and system-level disease shaped by dynamic interactions among malignant cells, stromal elements, the vasculature, the immune system, and the nervous system. In this context, tumors are not passive recipients of neural input, but active participants in the recruitment, remodeling, and exploitation of neural circuits that support tumor initiation, progression, metastasis, immune evasion, and resistance to therapy. Emerging work in cancer neuroscience has therefore shifted the field from a neuron-centric perspective toward an integrated model of the tumor microenvironment in which malignant cells help establish pathogenic neural niches. This review adopts a tumor-centric perspective to examine how cancer cells drive neoneurogenesis, engage in perineural invasion, and co-opt neural signaling and neuro-immune crosstalk to promote disease progression. It first distinguishes tumor-induced nerve growth and remodeling from perineural invasion as related but mechanistically distinct processes, then considers how tumor cell plasticity and neural mimicry enable malignant cells to acquire neuronal-like traits and exploit neural pathways. The review further explores how tumor-driven innervation shapes angiogenesis, immune modulation, therapeutic resistance, and minimal residual disease while also assessing emerging strategies designed to therapeutically target the tumor–nerve axis. By integrating these themes, the review highlights innervation not as a secondary feature of cancer, but as an active and potentially actionable dimension of tumor biology.