Mitochondria are membrane-bound cell organelles that undertake the majority of the energetic and metabolic processes within the cell. They are also responsible for mediating multiple apoptotic pathways, balancing redox charges, and scavenging reactive oxygen species. MicroRNAs, which are short, non-coding RNAs widely known for regulating gene expression at the post-transcriptional level, regulate many of these processes. The specific microRNAs that directly or indirectly control mitochondrial dynamics are called mitochondrial miRNAs (mitomiRs). The broadest classification of this type of ncRNA encompasses nuclear-encoded miRNAs that interact with cytoplasmatic mRNAs associated with mitochondrial activity. At the same time, a more specific subset comprises nuclear-encoded miRNAs that translocate into the mitochondria to interact with mRNAs inside of this organelle. Finally, the smallest group of mitomiRs includes those codified by mtDNA and can regulate endogenous mitochondrial transcripts or be transported into the cytoplasm to modulate circulating mRNAs. Regardless of the origin or action mechanism, mitomiRs have been recently recognized to have a key role in the progression of a variety of chronic disorders, such as neurodegenerative and cardiovascular diseases, diabetes, asthma, depression, and even cancer. All of these progressive pathologies have been tightly linked to mitochondrial dysregulation. They are further associated with an aberrant expression of specific miRNAs that regulate cellular metabolism, positioning mitomiRs as reliable biomarkers for diagnosing several chronic diseases. These molecular indicators have also provided insights into how these conditions progress, allowing for the development of different miRNA-based treatment strategies that target dysregulated mitochondrial-related genes, reestablishing their baseline activity and restricting further disease progression.

Background: Mesoporous titanium dioxide nanoparticles (mTiNPs) are known for their chemical stability, non-toxicity, antimicrobial and anticancer effects, as well as for their photocatalytic properties. When this material is subjected to UV radiation, its electronic structure shifts, and during that process, reactive oxygen species are generated, which in turn exert apoptotic events on the cancer cells. Objectives: We evaluated the cytotoxic effects of UV-irradiated mTiNPs on prostate cancer (PCa) cell line PC3 with the aim of demonstrating that the interaction between UV-light and mTiNPs positively impacts the nanomaterial’s cytotoxic efficiency. Moreover, we assessed the differential expression of key oncomiRs and tumor suppressor (TS) miRNAs, as well as their associated target genes, in cells undergoing this treatment. Methods: PBS-suspended mTiNPs exposed to 290 nm UV light were added at different concentrations to PC3 cells. Cell viability was determined after 24 h with a crystal violet assay. Then, the obtained IC₅₀ concentration of UV-nanomaterial was applied to a new PC3 cell culture, and the expression of a set of miRNAs and selected target genes was evaluated via qRT-PCR. Results: The cells exposed to photo-activated mTiNPs required 4.38 times less concentration of the nanomaterial than the group exposed to non-irradiated mTiNPs to achieve the half-maximal inhibition, demonstrating an improved cytotoxic performance of the UV-irradiated mTiNPs. Moreover, the expression of miR-18a-5p, miR-21-5p, and miR-221-5p was downregulated after the application of UV-mTiNPs, while TS miR-200a-5p and miR-200b-5p displayed an upregulated expression. Among the miRNA target genes, PTEN was found to be upregulated after the treatment, while BCL-2 and TP53 were underexpressed. Conclusions: Our cytotoxic outcomes coincided with previous reports performed in other cancer cell lines, strongly suggesting UV-irradiated mTiNPs as a promising nano-therapeutic approach against PCa. On the other hand, to the best of our knowledge, this is the first report exploring the impact of UV-irradiated mTiNPs on key onco- and TS microRNAs in PCa cells.

Skin aging is a multifactorial process influenced by intrinsic and extrinsic factors, including cellular senescence, photoaging, glycation, and impaired wound healing, all of which begin at birth. Recent epigenetic research has identified non-coding RNAs (ncRNAs), particularly microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), as key regulators of gene networks governing skin homeostasis, regeneration, and aging. However, the literature remains fragmented, lacking a cohesive framework that integrates ncRNA biogenesis, mechanistic function, and therapeutic relevance across aging pathways. This review consolidates current evidence on ncRNA-mediated regulation of skin aging, focusing on their roles in modulating oxidative stress, extracellular matrix remodeling, stem cell exhaustion, and inflammatory signaling. We highlight key ncRNAs such as miR-146a, miR-296-5p, lncRNA-H19, lncRNA-PVT1, and circRNA-406918, and their molecular targets including SIRT1, AQP3, NAMPT, TLR4 and CTSD, coordinating signaling via PI3K/mTOR, AMPK/NAD+ /SIRT, and ERK/p38 MAPK axes. We further address ncRNAs as diagnostic biomarkers and therapeutic candidates in precision dermatology and discuss the translational landscape, including delivery innovations and early-phase clinical studies. While preclinical models show strong promise, clinical applications remain limited, emphasizing the need for human-focused mechanistic and therapeutic research.

Insulin resistance (IR) is a key feature in the pathophysiology of metabolic disorders such as type 2 diabetes mellitus (T2DM) and obesity, both of which have a high prevalence in the Mexican population. Genetic predisposition plays a critical role in the development of IR, particularly through variants in carbohydrate metabolism genes. However, the specific contributions of these genetic factors in young Mexicans remain poorly characterized. This study aimed to identify associations between single nucleotide polymorphisms (SNPs) in carbohydrate metabolism-related genes and insulin resistance markers in a young Mexican population. Additionally, we sought to identify novel genetic variants that may contribute to metabolic risk and explore sex-specific genetic effects. A genome-wide association study was conducted on 455 urban college students from Mexico. A total of 430 SNPs related to carbohydrate metabolism were genotyped. Clinical markers of IR, including fasting glucose, insulin, the homeostasis model assessment for insulin resistance (HOMA-IR), body mass index (BMI), body fat percentage (BF%), and waist circumference (WC), were evaluated. Associations between SNPs and metabolic traits were analyzed using logistic regression models adjusted for relevant covariates. Bonferroni correction was applied to account for multiple testing. Several SNPs were significantly associated with IR-related traits. SNPs in glucose metabolism genes, including GCK (rs1799884), SLC2 A9 (rs1122141), and IDH3B (rs6037255), were linked to fasting glucose levels, with IDH3B showing the strongest effect (OR 12.17, p = 0.0144). Variants in insulin-related genes, such as SLC2 A9, PFKP (rs3814591), and SLC45 A1 (rs12132135), were associated with elevated insulin and HOMA-IR. Adiposity-related SNPs, including those in PDK3 (rs7889665), PGK1 (rs2076630), and IDH2 (rs62019177), influenced body fat percentage and BMI. Notably, the novel variant rs77487659 (PGLS) was significantly associated with IR, particularly in women (OR 5.5, p = 0.00005), highlighting a potential sex-specific effect. The SLC45 A1 variant rs12132135 demonstrated significant associations with multiple metabolic traits, including BMI, WC, and insulin resistance. This study provides a comprehensive genetic analysis of IR-related traits in young Mexicans, highlighting both previously reported and novel associations. The findings suggest that genetic predisposition plays an important role in metabolic risk, with potential implications for early screening and personalized interventions. Sex-specific effects emphasize the need for tailored approaches in genetic risk assessment. Future research should focus on functional validation of these SNPs and their integration into precision medicine strategies for metabolic disease prevention.