9 results on '"Farsetti, Antonella"'
Search Results
2. How epigenetics impacts on human diseases.
- Author
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Farsetti, Antonella, Illi, Barbara, and Gaetano, Carlo
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EPIGENETICS , *DRUG side effects , *GENE expression , *HUMAN abnormalities , *NUCLEOTIDE sequence - Abstract
• Epigenetics, a rapidly expanding field of biology, involves the study of changes in gene expression that don't stem from changes in the DNA sequence, but rather from chemical modifications of DNA and its associated proteins. • Epigenetic mechanisms can significantly influence gene expression, cell differentiation, tissue development, and susceptibility to diseases. • Understanding epigenetic changes is crucial for elucidating the role of environmental and lifestyle factors in health and disease, as well as the intergenerational transmission of phenotypes. • Recent studies indicate that epigenetics may play a vital role in a wide range of diseases, including cardiovascular disease, cancer, neurodevelopmental disorders, and neurodegenerative disorders. • Epigenetic modifications are potentially reversible, offering promising new therapeutic approaches for treating these diseases using epigenetic modulators. • Epigenetics also offers insights into disease pathogenesis and potential biomarkers for disease diagnosis and risk stratification. • However, there are potential risks associated with epigenetic interventions, including unintended consequences like adverse drug reactions, developmental abnormalities, and cancer. • Rigorous studies are necessary to minimize the risks associated with epigenetic therapies and to develop safe and effective interventions to improve human health. • The article provides a synthetic and historical view of the origin of epigenetics and highlights some of the most relevant achievements in the field. Epigenetics is a rapidly growing field of biology that studies the changes in gene expression that are not due to alterations in the DNA sequence but rather the chemical modifications of DNA and its associated proteins. Epigenetic mechanisms can profoundly influence gene expression, cell differentiation, tissue development, and disease susceptibility. Understanding epigenetic changes is essential to elucidate the mechanisms underlying the increasingly recognized role of environmental and lifestyle factors in health and disease and the intergenerational transmission of phenotypes. Recent studies suggest epigenetics may be critical in various diseases, from cardiovascular disease and cancer to neurodevelopmental and neurodegenerative disorders. Epigenetic modifications are potentially reversible and could provide new therapeutic avenues for treating these diseases using epigenetic modulators. Moreover, epigenetics provide insight into disease pathogenesis and biomarkers for disease diagnosis and risk stratification. Nevertheless, epigenetic interventions have the potential for unintended consequences and may potentially lead to increased risks of unexpected outcomes, such as adverse drug reactions, developmental abnormalities, and cancer. Therefore, rigorous studies are essential to minimize the risks associated with epigenetic therapies and to develop safe and effective interventions for improving human health. This article provides a synthetic and historical view of the origin of epigenetics and some of the most relevant achievements. [ABSTRACT FROM AUTHOR]
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- 2023
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3. Anacardic acid and thyroid hormone enhance cardiomyocytes production from undifferentiated mouse ES cells along functionally distinct pathways
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Re, Agnese, Nanni, Simona, Aiello, Aurora, Granata, Serena, Colussi, Claudia, Campostrini, Giulia, Spallotta, Francesco, Mattiussi, Stefania, Pantisano, Valentina, D’Angelo, Carmen, Biroccio, Annamaria, Rossini, Alessandra, Barbuti, Andrea, DiFrancesco, Dario, Trimarchi, Francesco, Pontecorvi, Alfredo, Gaetano, Carlo, and Farsetti, Antonella
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- 2016
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4. Epigenetic Signaling and RNA Regulation in Cardiovascular Diseases.
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Mongelli, Alessia, Atlante, Sandra, Bachetti, Tiziana, Martelli, Fabio, Farsetti, Antonella, and Gaetano, Carlo
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RNA ,CARDIOVASCULAR diseases ,RNA modification & restriction ,DNA structure ,SMALL molecules - Abstract
RNA epigenetics is perhaps the most recent field of interest for translational epigeneticists. RNA modifications create such an extensive network of epigenetically driven combinations whose role in physiology and pathophysiology is still far from being elucidated. Not surprisingly, some of the players determining changes in RNA structure are in common with those involved in DNA and chromatin structure regulation, while other molecules seem very specific to RNA. It is envisaged, then, that new small molecules, acting selectively on RNA epigenetic changes, will be reported soon, opening new therapeutic interventions based on the correction of the RNA epigenetic landscape. In this review, we shall summarize some aspects of RNA epigenetics limited to those in which the potential clinical translatability to cardiovascular disease is emerging [ABSTRACT FROM AUTHOR]
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- 2020
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5. The nuclear pore protein Nup153 associates with chromatin and regulates cardiac gene expression in dystrophic mdx hearts.
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Nanni, Simona, Re, Agnese, Ripoli, Cristian, Gowran, Aoife, Nigro, Patrizia, D'Amario, Domenico, Amodeo, Antonio, Crea, Filippo, Grassi, Claudio, Pontecorvi, Alfredo, Farsetti, Antonella, and Colussi, Claudia
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CHROMATIN ,GENE expression ,NUCLEAR pore complex ,HEART diseases ,EPIGENETICS - Abstract
Aims: Beyond the control of nuclear-cytoplasmic trafficking nucleoporins regulate gene expression and are involved in cardiac diseases. Notably, a number of cardiovascular disorders have been linked to alterations in epigenetic mechanisms. Here we aimed to determine the contribution of Nup153 to the epigenetic alterations occurring in cardiomyopathy of dystrophin-deficient mdx mice (C57BL/10ScSn-Dmd
mdx /J). Methods and results: Nup153 was lysine-acetylated and its expression was significantly increased at protein level in mdx hearts compared with controls. Accordingly, lysine acetyl transferase (KAT) activity associated with Nup153 was higher in mdx hearts paralleling increased binding with the lysine acetylases P300/CBP-associated factor (PCAF) and p300. Interestingly, Nup153 silencing in mdx organotypic heart tissue slices caused a reduction in PCAF- and p300-specific activities. Remarkably, the level of nitric oxide (NO), which is reduced in mdx mice, was important for KAT-dependent regulation of Nup153. In fact, treatment of mdx heart tissue with an NO donor or the KAT inhibitor anacardic acid normalized Nup153 protein expression. Nup153 was recruited to chromatin and regulated the transcription of genes involved in cardiac remodelling, including the actin-binding protein nexilin. Accordingly, nexilin protein expression was abrogated by Nup153 silencing in mdx organotypic cultures. Electrophysiological and molecular experiments revealed that Nup153 overexpression in normal cardiomyocytes increases Cav 1.2 calcium channel expression and function. Alterations in Nup153 protein expression and intracellular localization were also found in dystrophic cardiomyocytes derived from patient-specific induced pluripotent stem cells. Importantly, Nup153 up-regulation and increased acetylation were also found in the heart of Duchenne muscular dystrophy patients. Conclusions: Our data indicate that Nup153 is an epigenetic regulator which, upon altered NO signalling, mediates the activation of genes potentially associated with early dystrophic cardiac remodelling. [ABSTRACT FROM AUTHOR]- Published
- 2016
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6. NO points to epigenetics in vascular development.
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Illi, Barbara, Colussi, Claudia, Rosati, Jessica, Spallotta, Francesco, Nanni, Simona, Farsetti, Antonella, Capogrossi, Maurizio C., and Gaetano, Carlo
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NUCLEOTIDE sequence ,NITRIC oxide ,GENE targeting ,BLOOD-vessel development ,CARDIOVASCULAR diseases ,CELL differentiation ,LINEAGE - Abstract
Our understanding of epigenetic mechanisms important for embryonic vascular development and cardiovascular differentiation is still in its infancy. Although molecular analyses, including massive genome sequencing and/or in vitro/in vivo targeting of specific gene sets, has led to the identification of multiple factors involved in stemness maintenance or in the early processes of embryonic layers specification, very little is known about the epigenetic commitment to cardiovascular lineages. The object of this review will be to outline the state of the art in this field and trace the perspective therapeutic consequences of studies aimed at elucidating fundamental epigenetic networks. Special attention will be paid to the emerging role of nitric oxide in this field. [ABSTRACT FROM AUTHOR]
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- 2011
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7. Evidence for Biological Age Acceleration and Telomere Shortening in COVID-19 Survivors.
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Mongelli, Alessia, Barbi, Veronica, Gottardi Zamperla, Michela, Atlante, Sandra, Forleo, Luana, Nesta, Marialisa, Massetti, Massimo, Pontecorvi, Alfredo, Nanni, Simona, Farsetti, Antonella, Catalano, Oronzo, Bussotti, Maurizio, Dalla Vecchia, Laura Adelaide, Bachetti, Tiziana, Martelli, Fabio, La Rovere, Maria Teresa, and Gaetano, Carlo
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COVID-19 ,COVID-19 pandemic ,SARS-CoV-2 ,HEART fibrosis ,ANGIOTENSIN converting enzyme ,TELOMERES - Abstract
The SARS-CoV-2 infection determines the COVID-19 syndrome characterized, in the worst cases, by severe respiratory distress, pulmonary and cardiac fibrosis, inflammatory cytokine release, and immunosuppression. This condition has led to the death of about 2.15% of the total infected world population so far. Among survivors, the presence of the so-called persistent post-COVID-19 syndrome (PPCS) is a common finding. In COVID-19 survivors, PPCS presents one or more symptoms: fatigue, dyspnea, memory loss, sleep disorders, and difficulty concentrating. In this study, a cohort of 117 COVID-19 survivors (post-COVID-19) and 144 non-infected volunteers (COVID-19-free) was analyzed using pyrosequencing of defined CpG islands previously identified as suitable for biological age determination. The results show a consistent biological age increase in the post-COVID-19 population, determining a DeltaAge acceleration of 10.45 ± 7.29 years (+5.25 years above the range of normality) compared with 3.68 ± 8.17 years for the COVID-19-free population (p < 0.0001). A significant telomere shortening parallels this finding in the post-COVID-19 cohort compared with COVID-19-free subjects (p < 0.0001). Additionally, ACE2 expression was decreased in post-COVID-19 patients, compared with the COVID-19-free population, while DPP-4 did not change. In light of these observations, we hypothesize that some epigenetic alterations are associated with the post-COVID-19 condition, particularly in younger patients (< 60 years). [ABSTRACT FROM AUTHOR]
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- 2021
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8. The double life of cardiac mesenchymal cells: Epimetabolic sensors and therapeutic assets for heart regeneration.
- Author
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Cencioni, Chiara, Atlante, Sandra, Savoia, Matteo, Martelli, Fabio, Farsetti, Antonella, Capogrossi, Maurizio C., Zeiher, Andreas M., Gaetano, Carlo, and Spallotta, Francesco
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CARDIAC regeneration , *MESENCHYMAL stem cells , *DIABETES risk factors , *AGE factors in disease , *BIOSENSORS , *HEART fibrosis - Abstract
Organ-specific mesenchymal cells naturally reside in the stroma, where they are exposed to some environmental variables affecting their biology and functions. Risk factors such as diabetes or aging influence their adaptive response. In these cases, permanent epigenetic modifications may be introduced in the cells with important consequences on their local homeostatic activity and therapeutic potential. Numerous results suggest that mesenchymal cells, virtually present in every organ, may contribute to tissue regeneration mostly by paracrine mechanisms. Intriguingly, the heart is emerging as a source of different cells, including pericytes, cardiac progenitors, and cardiac fibroblasts. According to phenotypic, functional, and molecular criteria, these should be classified as mesenchymal cells. Not surprisingly, in recent years, the attention on these cells as therapeutic tools has grown exponentially, although only very preliminary data have been obtained in clinical trials to date. In this review, we summarized the state of the art about the phenotypic features, functions, regenerative properties, and clinical applicability of mesenchymal cells, with a particular focus on those of cardiac origin. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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9. Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health
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Sandra Atlante, Carlo Gaetano, Johanna Heid, Andreas M. Zeiher, Alessandro Cellerino, Antonella Farsetti, Stefan Guenther, Giulio Pompilio, Francesco Spallotta, Chiara Cencioni, Giuseppina Milano, Giacomo Rossi, Fabio Martelli, Alessandro Scopece, Thomas Braun, Valerio Azzimato, Mario Baumgart, Roberto Ripa, Carsten Kuenne, Heid, Johanna, Cencioni, Chiara, Ripa, Roberto, Baumgart, Mario, Atlante, Sandra, Milano, Giuseppina, Scopece, Alessandro, Kuenne, Carsten, Guenther, Stefan, Azzimato, Valerio, Farsetti, Antonella, Rossi, Giacomo, Braun, Thoma, Pompilio, Giulio, Martelli, Fabio, Zeiher, Andreas M, Cellerino, Alessandro, Gaetano, Carlo, and Spallotta, Francesco
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0301 basic medicine ,Aging ,lcsh:Medicine ,Cell biology ,Cardiovascular biology ,medicine.disease_cause ,Settore BIO/09 - Fisiologia ,fibroblast ,Muscle hypertrophy ,Transcriptome ,0302 clinical medicine ,Fibrosis ,lcsh:Science ,Zebrafish ,Multidisciplinary ,biology ,microRNA ,cardiovascular ,Fishes ,epigenetics ,Heart ,5-Methylcytosine/metabolism ,Animals ,Antagomirs/metabolism ,Cell Hypoxia ,Cell Line ,Collagen/metabolism ,DNA Methylation ,Echocardiography ,Fibroblasts/cytology ,Fibroblasts/metabolism ,Fishes/genetics ,Heart/physiology ,Humans ,MicroRNAs/antagonists & inhibitors ,MicroRNAs/genetics ,MicroRNAs/metabolism ,Myocardium/metabolism ,Oxidative Stress ,Up-Regulation ,5-Methylcytosine ,Collagen ,Cardiac function curve ,medicine.medical_specialty ,Article ,03 medical and health sciences ,Downregulation and upregulation ,Internal medicine ,medicine ,Myocardium ,lcsh:R ,Antagomirs ,Fibroblasts ,medicine.disease ,biology.organism_classification ,MicroRNAs ,030104 developmental biology ,Endocrinology ,lcsh:Q ,030217 neurology & neurosurgery ,Oxidative stress - Abstract
The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12–21 week (adult) and 28–40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O2 levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.
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- 2017
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