Current Pharmaceutical Design - Volume 32, Issue 13, 2026

Mitochondria are known as the powerhouse of eukaryotic cells. They play a crucial role in several biological processes and maintain cellular health. The ideal condition of mitochondria depends not only on their morphology but also on various micro-environmental factors, including pH, polarity, and temperature. Changes in these factors or malfunctions of mitochondrial species, such as Reactive Oxygen Species (ROS), active nitrogen species, metal cations, anions, and protons, can lead to several diseases in humans, including heart failure, kidney disorders, diabetes, Alzheimer’s disease, and Parkinson's disease. Therefore, monitoring Reactive Small Molecules (RSMs), maintaining micro-environmental factors, and estimating ROS levels in mitochondria are essential for understanding physiological behaviour and the pathogenesis of related diseases. Irregularities in mitochondrial function are closely linked to a range of clinical conditions, highlighting the importance of targeting mitochondria for therapeutic benefits. Over the last decade, numerous studies have focused on the development of small organic conjugated systems for mitochondrial imaging, utilizing optical signal transduction pathways. In this review, the design and synthetic strategies for small organic fluorophores conjugated with a pyridinium acceptor, their applications in mitochondrial imaging, and the detection of RSMs in mitochondria have been discussed. Studies have revealed that small-molecule fluorescent probes are being widely used for the detection and imaging of RSMs located in mitochondria. Moreover, this review covers the mechanistic insights, photophysical properties, biological characteristics of fluorophores, and therapeutic strategies targeting the mitochondria of human cells.

Emerging evidence reveals that interactions between the nervous system and tumor biology significantly influence cancer progression, metastasis, and therapeutic outcomes. Here, we elucidate the neurobiological mechanisms that underpin tumor development, highlighting the dynamic role of neural components within the tumor microenvironment (TME). Neural signals and structural adaptations in the TME stimulate tumorigenesis and enable cancer cell plasticity, mimicking neurodevelopmental processes. Astrocytic glial cells release neurotrophic factors that support metastatic colonization and enhance tumor cell survival. Notably, cancer cells can establish pseudo-tripartite synapses with neurons, promoting both proliferation and invasion. We explore the cancer-neural network interplay, emphasizing how axonal remodeling, circuit reorganization, and synaptic dysfunction not only drive tumor growth but also contribute to associated symptoms like seizures and chronic pain. Molecularly, mutations such as in PIK3CA and abnormalities in neurotransmitter signaling reveal how neurotumors communicate and adapt. Furthermore, metabolic stress responses from tumor cells can activate nociceptive neurons, sustaining malignant progression. Understanding these neurobiological interactions opens avenues for novel therapeutic strategies. Precision neuro-oncology may benefit from targeting neurotrophic signaling, synaptic pathways, and neuronal differentiation programs. Advances in biomarker research from neurotumors also contribute to improved diagnostic and prognostic tools. By integrating neuroscience insights into oncological frameworks, we propose a paradigm shift toward therapies that intercept the neural circuitry sustaining malignancies. This neuro-oncological approach holds promise in addressing aggressive cancer phenotypes and improving patient outcomes.

Atopic dermatitis (AD) is a common chronic inflammatory skin disorder affecting both children and adults, characterized by intense itching, erythema, and xerosis. The pathogenesis of AD is multifactorial, involving genetic predisposition, immune dysregulation, skin barrier dysfunction, and environmental factors. A growing body of evidence suggests that oxidative stress plays a critical role in AD, contributing to chronic inflammation, immune cell activation, and skin barrier disruption. Oxidative stress arises from an imbalance between Reactive Oxygen Species (ROS) production and antioxidant defenses, leading to cellular damage and the exacerbation of AD symptoms. Recent research has highlighted the potential of plant-derived bioactive compounds, particularly those with antioxidant properties, to mitigate oxidative stress and provide therapeutic benefits in AD. These compounds, including quercetin, resveratrol, curcumin, silymarin, baicalin, luteolin, and epigallocatechin gallate, not only neutralize ROS but also exhibit anti-inflammatory, immunomodulatory, and skin barrier-restoring effects. Natural antioxidants from plants offer a safer alternative to conventional treatments, which may have long-term side effects. This review provides a comprehensive overview of the mechanisms by which oxidative stress contributes to AD and examines the potential of plant-derived antioxidants in alleviating AD symptoms. The growing interest in these compounds underscores the need for further research to harness their full therapeutic potential in AD management.

The use of CRISPR-Cas9 to engineer cancer cell lines has made it possible to precisely examine how cancer cells react to different drugs and therapies. Some of the key improvements are in the use of Mediator Complex Subunit 12 (MED12)-knockout cells to study cell resistance to BRAF inhibitors, CRISPR models of epithelial-mesenchymal transition for breast cancer, and pharmacogenomic analysis in various cancer cell lines. CRISPR is used in immunotherapy to help Chimeric Antigen Receptor T (CAR-T) cells function better by disrupting the immune checkpoints like Programmed Cell Death Protein 1 (PD-1) and Cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and to adapt T cells to react with various antigens. As a result of these innovations, it is now possible to track how cancers like non-small cell lung cancer (NSCLC) and ovarian cancer evolve, change their epigenetic features, and find strategies to reverse their resistance. Moving forward, integrating AI analytics, single-cell multi-omics, patient-derived organoids, and CRISPR mechanisms will help improve precision oncology and speed up effective treatment planning.