Carmen Marino is a Ph.D student at the University of Salerno. She gratuated in Science Biologists at the University of Sannio and specialized with honors in Biology at University of Salerno. From January to October 2020 carried out research, at the laboratory of Pharmaceutical Chemistry of Professor Anna Maria D'Ursi, within the project called "Fighting cancer resistance: integrated multidisciplinary platform for a project innovative technology to oncotherapies". Currently enrolled in the third year of PhD in Pharmaceutical Sciences, she dedicates herself to Research "Metabolomics approach in the study of molecular mechanisms of pathologies and in identification of new pharmacological targets".
EDUCATION
She graduated in Science Biologists at the University of Sannio and specialized with honors in Biology at University of Salerno. From January to October 2020 carried out research, at the laboratory of Pharmaceutical Chemistry of Professor Anna Maria D'Ursi, within the project called "Fighting cancer resistance: integrated multidisciplinary platform for a project innovative technology to oncotherapies". She holds a PhD in pharmaceutical sciences and is currently a research fellow at UNISA
RESEARCH INTERESTS
Carmen has focused her studies on biology field, in particular in omics techniques. Since her thesis period she has focused on the characterization of metabolomic profiles obtained through the analysis of biofluids and tissues with NMR spectroscopy.
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Scopus Publications
Scopus Publications
Untargeted 1H NMR-based metabolomics unveils distinct circulating biochemical signatures between treatment-resistant and non-treatment-resistant schizophrenia patients: a pilot study Carmen Marino, Siwei Zhang, Giuseppe De Simone, Manuela Grimaldi, Anna Di Maio, Felice Iasevoli, Francesco Errico, Anna Maria D’Ursi, Andrea de Bartolomeis, Alessandro Usiello Translational Psychiatry, 2026 Schizophrenia is a severe psychiatric disorder that affects approximately 1% of the population. Despite the availability of antipsychotic therapies, about 30% of patients develop treatment-resistant schizophrenia (TRS), defined by a lack of response to at least two different antipsychotic trials. Although several genetic and environmental factors have been proposed to explain treatment resistance, metabolomic studies investigating circulating metabolites in TRS remain limited. In this pilot cross-sectional study, we conducted untargeted 1H NMR-based metabolomics to profile serum metabolites in TRS versus non-TRS patients. Notably, multivariate analysis revealed distinct serum metabolome profiles between the two groups. Additionally, Variable Importance in Projection (VIP) analysis and robust volcano plots showed significant differences between TRS versus non-TRS patients in metabolites involved in lipid and amino acid metabolism. Specifically, serine and glycine emerged as key discriminating molecules, prompting a complementary targeted HPLC analysis in the same serum samples. Although no significant group differences were observed in L-serine, D-serine, the D-serine/total serine ratio, or glycine levels, we found a positive correlation between D-serine levels and cognitive performance, particularly in the area of executive function, across the entire patient cohort. Additionally, a significant correlation between glycine and disorganization symptoms was found selectively in TRS patients. In conclusion, our study offers new insights into potential biomarkers for TRS, highlighting serine-glycine pathway as a possible crossroad between systemic dysmetabolism, NMDA receptor dysfunction, and cognitive impairment in TRS.
Epigenetic alterations of AKT1 orchestrate a metabolic reprogramming in advanced lipedema: translational insights from an integrated multi-omics study Biagio Santella, Annamaria Salvati, Alexander Papp, Annamaria D’Ursi, Domenico Memoli, Monica Mingo, Christoph Pulai, Carmen Marino, Luca Rastrelli, Maria D’Elia, Giovanni Nassa, Luigi Schiavo Journal of Translational Medicine, 2026 lipedema is a chronic, progressive adipose disorder predominantly affecting women, characterized by painful, symmetrical subcutaneous fat accumulation, and typically resistant to lifestyle interventions. The pathophysiology of advanced-stage lipedema remains poorly defined, and no validated biomarkers or targeted therapies are currently available. in this observational study, we applied a comprehensive multi-omics approach to dissect the molecular and metabolic alterations underlying late-stage lipedema. Genome-wide DNA methylation profiling identified over 5,000 differentially methylated CpG sites affecting genes involved in receptor tyrosine kinase signaling, phospho-metabolism, and immune pathways. Transcriptomic analysis revealed profound downregulation of mitochondrial functions, including oxidative phosphorylation, the TCA cycle, and fatty acid β-oxidation, alongside disruption of the sirtuin pathway and extracellular matrix remodeling. Integrative analysis pinpointed AKT1 as a central regulatory node: its promoter region was hypomethylated, correlating with increased gene expression and protein phosphorylation. Metabolomic profiling confirmed AKT1-linked metabolic dysregulation, including altered levels of L-arginine, NADP+, ATP, guanosine, glycerol, and glutamate, indicating impaired redox balance and energy metabolism. Trans-omic network analysis positioned AKT1 at the intersection of multiple dysregulated pathways, suggesting its key role in advanced-stage lipedema. the consistent enhancing of AKT pathway signaling across omic layers highlights its potential not only as a biomarker for disease stratification but also as a putative druggable target for therapeutic intervention. These findings offer new mechanistic insights into lipedema pathophysiology and provide a rationale for future personalized treatment strategies guided by AKT1-centric molecular profiling. Epigenetic profiling reveals AKT1 promotes hypomethylation and overexpression in advanced-stage lipedema. Transcriptomic analysis shows mitochondrial dysfunction, with downregulation of OXPHOS, TCA cycle, and β-oxidation genes. Untargeted metabolomics identifies AKT1-associated alterations in redox balance, amino acid metabolism, and energy production. Trans-omic network analysis positions AKT1 as a central regulatory hub linking epigenetic, transcriptional, and metabolic changes. Integrated multi-omics profiling supports AKT1 as a candidate biomarker and therapeutic target in advanced-stage lipedema.
Analyzing Nicotine Action Against Amyloid Toxicity by NMR-Pharmacometabolomics: An Exploratory Study Enza Napolitano, Carmen Marino, Manuela Grimaldi, Michela Buonocore, Angelo Santoro, Anna Maria D'Ursi NMR in Biomedicine, 2026 Alzheimer's disease ( AD ) is the primary neurodegenerative disease spread worldwide. One of the main histopathological hallmarks of AD is the deposition of amyloid plaques in the brain. Despite some epidemiological studies demonstrating that cigarette smoke is a factor in predisposing people to AD , nicotine, the principal alkaloid of Nicotiana Tobacco , has been widely studied for its ability to improve cognitive performance, both in animal models and in human studies. Several hypotheses have been proposed to explain the mechanism of action underlying the beneficial effect of nicotine in AD ; however, this is still questioned. To gain new insights into the molecular mechanism underlying nicotine's neuroprotective action in AD , we performed NMR metabolomics on SH‐SY5Y neuroblastoma cells treated with Aβ(1–42) in the presence of nicotine. Our data show that the neuroprotective action of nicotine resides in its ability to restore the systemic unbalanced metabolism associated with AD . In particular, nicotine reverses most Aβ(1–42)‐induced metabolic impairments, including those related to amino acid metabolism, especially neurotransmission, as well as alterations in energy and membrane phospholipid metabolism.
Cell Surface Markers of Mesenchymal Stem Cells: Current Knowledge and Advances in Characterization Technologies Angelo Santoro, Manuela Grimaldi, Carmen Marino, Enza Napolitano, Michela Buonocore, Anna Maria D’Ursi Life, 2026 Mesenchymal stem cells (MSCs) are pivotal in regenerative medicine due to their high differentiation potential and therapeutic versatility. MSCs are multipotent cells capable of differentiating into adipocytes, chondroblasts, osteoblasts, and, under specific conditions, neural, myocyte, and epidermal lineages. This cell type contributes to tissue repair, immunomodulation, and regenerative therapies for cardiac, orthopedic, and hematological disorders. Accurate identification and characterization of these stem cells are essential for both research and clinical applications. MSCs are typically defined by plastic adherence, expression of surface markers CD105, CD73, and CD90, low or absent expression of hematopoietic markers (CD45, CD34), and in vitro differentiation potential. Understanding the expression patterns and functional relevance of these surface markers is critical for improving isolation strategies, enhancing therapeutic efficacy, and minimizing adverse effects. This review provides a comprehensive overview of the principal surface markers of MSCs, highlighting their significance in stem cell biology and clinical translation.
1H-NMR-based metabolomics identifies disrupted betaine metabolism as distinct serum signature of pre-frailty Carmen Marino, Alberto Imarisio, Clara Gasparri, Enza Napolitano, Anna Di Maio, Micol Avenali, Gabriele Buongarzone, Caterina Galandra, Marta Picascia, Manuela Grimaldi, Francesco Errico, Mariangela Rondanelli, Anna Maria D’Ursi, Enza Maria Valente, Alessandro Usiello Npj Aging, 2025 Increasing evidence suggests that frailty results from a complex age-associated metabolic decline. Here, we investigated the serum metabolomic profile of a well-characterized cohort of elderly subjects encompassing the whole fit-to-frail continuum. Enrichment analyses revealed a complex dysregulation of amino acids and energy metabolism in both pre-frail and frail participants. Remarkably, upregulated betaine levels emerged as a specific biochemical signature of pre-frail females, holding promise for the development of novel targeted interventions.
Independent serum metabolomics approaches identify disrupted glutamic acid and serine metabolism in Parkinson’s disease patients Jacopo Gervasoni, Carmen Marino, Alberto Imarisio, Lavinia Santucci, Enza Napolitano, Tommaso Nuzzo, Isar Yahyavi, Micol Avenali, Michela Cicchinelli, Gabriele Buongarzone, Caterina Galandra, Marta Picascia, Manuela Grimaldi, Claudio Pacchetti, Francesco Errico, Anna Maria D’Ursi, Andrea Urbani, Enza Maria Valente, Alessandro Usiello Npj Parkinson S Disease, 2025 Whether distinct blood metabolomic profiles can distinguish Parkinson’s disease (PD) patients from healthy controls (HC) is still a matter of debate. Here, we employed ¹H-NMR and UPLC/MS analyses on serum samples from a cohort of PD patients and HC. Compared to HC, PD patients showed: (1) higher glutamine, serine, pyruvate and lower α-ketoglutarate levels ( 1 H-NMR); (2) higher glycine and lower glutamic acid concentrations (UPLC/MS). Several pathways associated with amino acids, mitochondrial and antioxidant metabolism emerged as dysregulated in PD. Our findings highlight a prominent disruption of cellular bioenergetic pathways and amino acid homeostasis in PD.
Effects of Nicotine on SH-SY5Y Cells: An NMR-Based Metabolomic Study Enza Napolitano, Carmen Marino, Manuela Grimaldi, Michela Buonocore, Anna Maria D’Ursi Metabolites, 2025 Background/Objectives: Nicotine is a naturally occurring alkaloid primarily found in Nicotiana tabacum. This phytochemical is well known for its addictive properties, and its consumption—particularly through tobacco smoking—is strongly associated with an increased risk of malignancies, metabolic dysfunctions, and cardiovascular as well as respiratory diseases. Despite these adverse effects, several studies have also reported beneficial actions of nicotine, including the enhancement of cognitive functions in several neurodegenerative diseases. Methods: To better elucidate the multiple effects of nicotine and clarify their underlying mechanisms, we performed an NMR-based metabolomic analysis of SH-SY5Y neuroblastoma cells exposed to nicotine action. Results: Our results indicate that nicotine modulates mitochondrial function and membrane turnover, thereby influencing mitochondrial bioenergetics, synaptic plasticity, and connectivity. Conclusions: Collectively, these findings may contribute, at least in part, to explaining the neuroprotective effects of nicotine described in preclinical models of neurodegenerative disease.
Modulation of Gut Bacterial and Fungal Microbiota in Fibromyalgia Patients Following a Carb-Free Oloproteic Diet: Evidence for Candida Suppression and Symptom Improvement Giuseppe Castaldo, Maria D’Elia, Mariagrazia De Prisco, Veronica Folliero, Carmen Marino, Annamaria D’Ursi, Gianluigi Franci, Luca Rastrelli Microorganisms, 2025 Fibromyalgia (FM) is a complex chronic syndrome characterized by widespread pain, fatigue, and gastrointestinal complaints. Clinical observations and preliminary metabolomic data suggest a possible link between symptom severity and intestinal dysbiosis, including fungal overgrowth. This study investigates whether a carb-free oloproteic diet can beneficially modulate the gut microbiota in FM patients. Thirty-four female patients with diagnosed FM were enrolled in a controlled, parallel-arm nutritional intervention. Group FM1 (n = 22) followed a 45-day carb-free oloproteic diet followed by a 45-day low-glycemic (LOGI) diet. Group FM2 (n = 12) received a continuous LOGI diet for 90 days. They were collected at baseline (T0), after 45 days (T45), and at 90 days (T90). Microbial profiles were analyzed by 16S and 18S rRNA gene sequencing to assess bacterial and fungal composition. In FM1, the oloproteic phase led to a marked reduction in fungal abundance (Ascomycota) and an increase in butyrate-producing bacteria such as Faecalibacterium and Roseburia. These changes were partially reversed after the LOGI phase. In FM2, no significant microbiota shifts were observed. Clinical improvements paralleled microbiota modulation only in FM1. The carb-free oloproteic diet may support gut microbial rebalancing in FM, particularly through transient suppression of fungal overgrowth. These findings support further investigation into nutritional strategies targeting dysbiosis in FM management.
Disclose ATP-synthase as a protein target of the antimicrobial peptide RiLK1 in Escherichia coli: An alternative receptor-mediated bactericidal mechanism Alessandra Capuano, Ennio Cocca, Angela Michela Immacolata Montone, Gilda D'Urso, Sonia Del Prete, Bruna Agrillo, Carmen Marino, Gianna Palmieri, Agostino Casapullo Food Chemistry, 2025 In this study, we investigated the mechanism of action of the 10-aminoacid RiLK1 peptide against Escherichia coli (strain ATCC 25922), both in vitro and in contaminated meat matrices. Therefore, a mass spectrometry-based functional proteomics platform was employed to identify specific molecular targets of RiLK1 in a membrane protein-enriched E. coli lysate and to obtain information on their interaction mechanism. This target deconvolution approach combines MS-limited proteolysis techniques, like Drug Affinity Responsive Target Stability (DARTS) and targeted-limited Proteolysis coupled with Mass Spectrometry (t-LiP-MS). The b and δ subunits of the multimeric enzymatic complex ATP synthase, the smallest known biological nanomotor found in all cells, were identified as the relevant RiLK1 membrane protein targets. Extensive molecular docking and biochemical analyses validated and improved the suggested interaction profile. These unique findings could rationally explain the relevant RiLK1 bactericidal effects against E. coli strains, suggesting its potential application in food safety and preservation. • MS-based functional proteomics in target discovery of antimicrobial peptides. • Escherichia coli ATP synthase as a protein target of the decapeptide RiLK1. • RiLK1 inhibition mechanism of Escherichia coli by proteomics and molecular docking. • RilK1, a short and non-toxic, arginine-rich antimicrobial peptide for food preservation.
Impact of a Formulation Containing Chaga Extract, Coenzyme Q10, and Alpha-Lipoic Acid on Mitochondrial Dysfunction and Oxidative Stress: NMR Metabolomic Insights into Cellular Energy Maria D’Elia, Carmen Marino, Rita Celano, Enza Napolitano, Chiara Colarusso, Rosalinda Sorrentino, Anna Maria D’Ursi, Luca Rastrelli Antioxidants, 2025 Objectives: The aim of this study was to evaluate the impact of a novel antioxidant formulation (RE:PAIR, RP-25) containing CoQ10, alpha-lipoic acid, and Chaga extract on mitochondrial dysfunction and oxidative stress. To explore the activity of the formulation on neuronal cells, we explored cell metabolism and its activity as an antioxidant, using a combination of NMR-based metabolomics and UHPLC-HRMS analytical techniques. Methods: SH-SY5Y neuroblastoma cells were treated with RP-25, and cell viability was assessed via CCK-8 assay. Metabolomic profiles of the treated and untreated cells were analyzed by 1D-NMR, providing insights into both intracellular metabolites (endometabolome) and excreted metabolites (exometabolome). Additionally, a UHPLC-HRMS method was developed for quality control and analysis of the RP-25 formulation. Multivariate statistical approaches, including PLS-DA and volcano plot analyses, were used to identify key metabolic changes. Changes in mitochondrial membrane potential were assessed by means of TMRE assay, while radical oxygen species (ROS) were measured by means of the DCHF assay. Results: RP-25 treatment did not affect cell viability but significantly increased metabolic pathways, including amino acid biosynthesis, oxidative phosphorylation, and glycolysis. Higher levels of ATP, glutamate, tyrosine, and proline were observed in treated cells than in control cells, indicating enhanced cellular energy production, as also proved by the increased stability of the mitochondrial membrane after RP-25 treatment, an index of preserved mitochondrial functions. In support, the formulation RP-25 showed antioxidant activity when cells underwent peroxide oxygen stimulation. This effect was mainly due to the combination of Chaga, CoQ10, and ALA, main components of the RP25 formulation. Moreover, the analysis of enriched pathways highlighted that RP formulation influenced mitochondrial energy and oxidative stress response. Conclusions: RP-25 demonstrated biological activity in that it mitigated mitochondrial dysfunction and oxidative stress in neuronal cells, with potential implications in neuronal diseases associated with dysfunctional mitochondria.
Investigating the Effectiveness of a Carb-Free Oloproteic Diet in Fibromyalgia Treatment Giuseppe Castaldo, Carmen Marino, Mariangela Atteno, Maria D’Elia, Imma Pagano, Manuela Grimaldi, Aurelio Conte, Paola Molettieri, Angelo Santoro, Enza Napolitano, Ilaria Puca, Mariangela Raimondo, Chiara Parisella, Anna Maria D’Ursi, Luca Rastrelli Nutrients, 2024
SMN deficiency perturbs monoamine neurotransmitter metabolism in spinal muscular atrophy Valeria Valsecchi, Francesco Errico, Valentina Bassareo, Carmen Marino, Tommaso Nuzzo, Paola Brancaccio, Giusy Laudati, Antonella Casamassa, Manuela Grimaldi, Adele D’Amico, Manolo Carta, Enrico Bertini, Giuseppe Pignataro, Anna Maria D’Ursi, Alessandro Usiello Communications Biology, 2023
Exploiting the Features of Short Peptides to Recognize Specific Cell Surface Markers Michela Buonocore, Manuela Grimaldi, Angelo Santoro, Verdiana Covelli, Carmen Marino, Enza Napolitano, Sara Novi, Mario Felice Tecce, Elena Ciaglia, Francesco Montella, Valentina Lopardo, Valeria Perugini, Matteo Santin, Anna Maria D’Ursi International Journal of Molecular Sciences, 2023
Nusinersen Induces Disease-Severity-Specific Neurometabolic Effects in Spinal Muscular Atrophy Francesco Errico, Carmen Marino, Manuela Grimaldi, Tommaso Nuzzo, Valentina Bassareo, Valeria Valsecchi, Chiara Panicucci, Elia Di Schiavi, Tommaso Mazza, Claudio Bruno, Adele D’Amico, Manolo Carta, Anna Maria D’Ursi, Enrico Bertini, Livio Pellizzoni, Alessandro Usiello Biomolecules, 2022
