EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress
<p>Diabetes-associated complications, such as retinopathy, nephropathy, cardiomyopathy, and atherosclerosis, the main consequences of long-term hyperglycemia, often lead to organ dysfunction, disability, and increased mortality. A common denominator of these complications is the myofibroblast-...
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2021
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| author | Roberta Giordo (299595) |
| author2 | Yusra M. A. Ahmed (16442006) Hilda Allam (16442007) Salah Abusnana (7956476) Lucia Pappalardo (364076) Gheyath K. Nasrallah (2182598) Arduino Aleksander Mangoni (16442013) Gianfranco Pintus (91638) |
| author2_role | author author author author author author author |
| author_facet | Roberta Giordo (299595) Yusra M. A. Ahmed (16442006) Hilda Allam (16442007) Salah Abusnana (7956476) Lucia Pappalardo (364076) Gheyath K. Nasrallah (2182598) Arduino Aleksander Mangoni (16442013) Gianfranco Pintus (91638) |
| author_role | author |
| dc.creator.none.fl_str_mv | Roberta Giordo (299595) Yusra M. A. Ahmed (16442006) Hilda Allam (16442007) Salah Abusnana (7956476) Lucia Pappalardo (364076) Gheyath K. Nasrallah (2182598) Arduino Aleksander Mangoni (16442013) Gianfranco Pintus (91638) |
| dc.date.none.fl_str_mv | 2021-05-19T06:00:00Z |
| dc.identifier.none.fl_str_mv | 10.3389/fcell.2021.683594 |
| dc.relation.none.fl_str_mv | https://figshare.com/articles/journal_contribution/EndMT_Regulation_by_Small_RNAs_in_Diabetes-Associated_Fibrotic_Conditions_Potential_Link_With_Oxidative_Stress/23575839 |
| dc.rights.none.fl_str_mv | CC BY 4.0 info:eu-repo/semantics/openAccess |
| dc.subject.none.fl_str_mv | Biological sciences Biochemistry and cell biology Biomedical and clinical sciences Clinical sciences Medical biochemistry and metabolomics EndMT miRNAs diabetes fibrosis oxidative stress |
| dc.title.none.fl_str_mv | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress |
| dc.type.none.fl_str_mv | Text Journal contribution info:eu-repo/semantics/publishedVersion text contribution to journal |
| description | <p>Diabetes-associated complications, such as retinopathy, nephropathy, cardiomyopathy, and atherosclerosis, the main consequences of long-term hyperglycemia, often lead to organ dysfunction, disability, and increased mortality. A common denominator of these complications is the myofibroblast-driven excessive deposition of extracellular matrix proteins. Although fibroblast appears to be the primary source of myofibroblasts, other cells, including endothelial cells, can generate myofibroblasts through a process known as endothelial to mesenchymal transition (EndMT). During EndMT, endothelial cells lose their typical phenotype to acquire mesenchymal features, characterized by the development of invasive and migratory abilities as well as the expression of typical mesenchymal products such as α-smooth muscle actin and type I collagen. EndMT is involved in many chronic and fibrotic diseases and appears to be regulated by complex molecular mechanisms and different signaling pathways. Recent evidence suggests that small RNAs, in particular microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), are crucial mediators of EndMT. Furthermore, EndMT and miRNAs are both affected by oxidative stress, another key player in the pathophysiology of diabetic fibrotic complications. In this review, we provide an overview of the primary redox signals underpinning the diabetic-associated fibrotic process. Then, we discuss the current knowledge on the role of small RNAs in the regulation of EndMT in diabetic retinopathy, nephropathy, cardiomyopathy, and atherosclerosis and highlight potential links between oxidative stress and the dyad small RNAs-EndMT in driving these pathological states. </p> <h2>Other Information</h2> <p>Published in: Frontiers in Cell and Developmental Biology<br> License: <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank">https://creativecommons.org/licenses/by/4.0/</a><br> See article on publisher's website: <a href="http://dx.doi.org/10.3389/fcell.2021.683594" target="_blank">http://dx.doi.org/10.3389/fcell.2021.683594 </a></p> |
| eu_rights_str_mv | openAccess |
| id | Manara2_471d36564d5bdabe23e4ff96efd5d6f3 |
| identifier_str_mv | 10.3389/fcell.2021.683594 |
| network_acronym_str | Manara2 |
| network_name_str | Manara2 |
| oai_identifier_str | oai:figshare.com:article/23575839 |
| publishDate | 2021 |
| repository.mail.fl_str_mv | |
| repository.name.fl_str_mv | |
| repository_id_str | |
| rights_invalid_str_mv | CC BY 4.0 |
| spelling | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative StressRoberta Giordo (299595)Yusra M. A. Ahmed (16442006)Hilda Allam (16442007)Salah Abusnana (7956476)Lucia Pappalardo (364076)Gheyath K. Nasrallah (2182598)Arduino Aleksander Mangoni (16442013)Gianfranco Pintus (91638)Biological sciencesBiochemistry and cell biologyBiomedical and clinical sciencesClinical sciencesMedical biochemistry and metabolomicsEndMTmiRNAsdiabetesfibrosisoxidative stress<p>Diabetes-associated complications, such as retinopathy, nephropathy, cardiomyopathy, and atherosclerosis, the main consequences of long-term hyperglycemia, often lead to organ dysfunction, disability, and increased mortality. A common denominator of these complications is the myofibroblast-driven excessive deposition of extracellular matrix proteins. Although fibroblast appears to be the primary source of myofibroblasts, other cells, including endothelial cells, can generate myofibroblasts through a process known as endothelial to mesenchymal transition (EndMT). During EndMT, endothelial cells lose their typical phenotype to acquire mesenchymal features, characterized by the development of invasive and migratory abilities as well as the expression of typical mesenchymal products such as α-smooth muscle actin and type I collagen. EndMT is involved in many chronic and fibrotic diseases and appears to be regulated by complex molecular mechanisms and different signaling pathways. Recent evidence suggests that small RNAs, in particular microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), are crucial mediators of EndMT. Furthermore, EndMT and miRNAs are both affected by oxidative stress, another key player in the pathophysiology of diabetic fibrotic complications. In this review, we provide an overview of the primary redox signals underpinning the diabetic-associated fibrotic process. Then, we discuss the current knowledge on the role of small RNAs in the regulation of EndMT in diabetic retinopathy, nephropathy, cardiomyopathy, and atherosclerosis and highlight potential links between oxidative stress and the dyad small RNAs-EndMT in driving these pathological states. </p> <h2>Other Information</h2> <p>Published in: Frontiers in Cell and Developmental Biology<br> License: <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank">https://creativecommons.org/licenses/by/4.0/</a><br> See article on publisher's website: <a href="http://dx.doi.org/10.3389/fcell.2021.683594" target="_blank">http://dx.doi.org/10.3389/fcell.2021.683594 </a></p>2021-05-19T06:00:00ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.3389/fcell.2021.683594https://figshare.com/articles/journal_contribution/EndMT_Regulation_by_Small_RNAs_in_Diabetes-Associated_Fibrotic_Conditions_Potential_Link_With_Oxidative_Stress/23575839CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/235758392021-05-19T06:00:00Z |
| spellingShingle | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress Roberta Giordo (299595) Biological sciences Biochemistry and cell biology Biomedical and clinical sciences Clinical sciences Medical biochemistry and metabolomics EndMT miRNAs diabetes fibrosis oxidative stress |
| status_str | publishedVersion |
| title | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress |
| title_full | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress |
| title_fullStr | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress |
| title_full_unstemmed | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress |
| title_short | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress |
| title_sort | EndMT Regulation by Small RNAs in Diabetes-Associated Fibrotic Conditions: Potential Link With Oxidative Stress |
| topic | Biological sciences Biochemistry and cell biology Biomedical and clinical sciences Clinical sciences Medical biochemistry and metabolomics EndMT miRNAs diabetes fibrosis oxidative stress |