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  1. Article ; Online: Letter by Belmadani and Matrougui Regarding Article, "Integrated Stress Response Couples Mitochondrial Protein Translation With Oxidative Stress Control".

    Belmadani, Souad / Matrougui, Khalid

    Circulation

    2022  Volume 145, Issue 14, Page(s) e802–e803

    MeSH term(s) Humans ; Mitochondrial Proteins/genetics ; Oxidation-Reduction ; Oxidative Stress ; Protein Biosynthesis
    Chemical Substances Mitochondrial Proteins
    Language English
    Publishing date 2022-04-04
    Publishing country United States
    Document type Letter ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.121.058242
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui IV Zs.60: Show issues Location:
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  2. Article ; Online: Role of High Mobility Group Box 1 in Cardiovascular Diseases.

    Belmadani, Souad / Matrougui, Khalid

    Inflammation

    2022  Volume 45, Issue 5, Page(s) 1864–1874

    Abstract: High Mobility Group Box 1 (HMGB1) is a ubiquitous, highly conserved nuclear and cytosolic protein that has diverse biological roles depending on its cellular location and posttranslational modifications. The HMGB1 is localized in the nucleus but can be ... ...

    Abstract High Mobility Group Box 1 (HMGB1) is a ubiquitous, highly conserved nuclear and cytosolic protein that has diverse biological roles depending on its cellular location and posttranslational modifications. The HMGB1 is localized in the nucleus but can be translocated to the cytoplasm to modulate the intracellular signaling and eventually secreted outside the cells. It is widely established that HMGB1 plays a key role in inflammation; however, the role of HMGB1 in the cardiovascular diseases is not well understood. In this review, we will discuss the latest reports on the pathophysiological link between HMGB1 and cardiovascular complications, with special emphasis on the inflammation. Thus, the understanding of the role of HMGB1 may provide new insights into developing new HMGB1-based therapies.
    MeSH term(s) Cardiovascular Diseases ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; HMGB1 Protein/metabolism ; Humans ; Inflammation/metabolism
    Chemical Substances HMGB1 Protein
    Language English
    Publishing date 2022-04-07
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 434408-x
    ISSN 1573-2576 ; 0360-3997
    ISSN (online) 1573-2576
    ISSN 0360-3997
    DOI 10.1007/s10753-022-01668-3
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  3. Article: Ac-SDKP attenuates ER stress-stimulated collagen production in cardiac fibroblasts by inhibiting CHOP-mediated NF-κB expression.

    Suhail, Hamid / Peng, Hongmei / Matrougui, Khalid / Rhaleb, Nour-Eddine

    Frontiers in pharmacology

    2024  Volume 15, Page(s) 1352222

    Abstract: Inflammation and cardiac fibrosis are prevalent pathophysiologic conditions associated with hypertension, cardiac remodeling, and heart failure. Endoplasmic reticulum (ER) stress triggers the cells to activate unfolded protein responses (UPRs) and ... ...

    Abstract Inflammation and cardiac fibrosis are prevalent pathophysiologic conditions associated with hypertension, cardiac remodeling, and heart failure. Endoplasmic reticulum (ER) stress triggers the cells to activate unfolded protein responses (UPRs) and upregulate the ER stress chaperon, enzymes, and downstream transcription factors to restore normal ER function. The mechanisms that link ER stress-induced UPRs upregulation and NF-κB activation that results in cardiac inflammation and collagen production remain elusive. N-Acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a natural tetrapeptide that negatively regulates inflammation and fibrosis, has been reported. Whether it can inhibit ER stress-induced collagen production in cardiac fibroblasts remains unclear. Thus, we hypothesized that Ac-SDKP attenuates ER stress-stimulated collagen production in cardiac fibroblasts by inhibiting CHOP-mediated NF-κB expression. We aimed to study whether Ac-SDKP inhibits tunicamycin (TM)-induced ER stress signaling, NF-κB signaling, the release of inflammatory cytokine interleukin-6, and collagen production in human cardiac fibroblasts (HCFs). HCFs were pre-treated with Ac-SDKP (10 nM) and then stimulated with TM (0.25 μg/mL). We found that Ac-SDKP inhibits TM-induced collagen production by attenuating ER stress-induced UPRs upregulation and CHOP/NF-κB transcriptional signaling pathways. CHOP deletion by specific shRNA maintains the inhibitory effect of Ac-SDKP on NF-κB and type-1 collagen (Col-1) expression at both protein and mRNA levels. Attenuating ER stress-induced UPR sensor signaling by Ac-SDKP seems a promising therapeutic strategy to combat detrimental cardiac inflammation and fibrosis.
    Language English
    Publishing date 2024-03-01
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2587355-6
    ISSN 1663-9812
    ISSN 1663-9812
    DOI 10.3389/fphar.2024.1352222
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Disrupting Interleukin 12 Improves Microvascular Endothelial Function in Type 2 Diabetes Through ER Stress CHOP and Oxidative Stress Mechanisms.

    Radwan, Eman / Belmadani, Souad / Matrougui, Khalid

    Diabetes, metabolic syndrome and obesity : targets and therapy

    2022  Volume 15, Page(s) 2633–2642

    Abstract: Purpose: Vascular endothelial dysfunction is well established in type 2 diabetes. Interleukin-12 (IL-12) and endoplasmic reticulum (ER) stress are up-regulated in type 2 diabetic patients and animal models of type 2 diabetes. However, the role and ... ...

    Abstract Purpose: Vascular endothelial dysfunction is well established in type 2 diabetes. Interleukin-12 (IL-12) and endoplasmic reticulum (ER) stress are up-regulated in type 2 diabetic patients and animal models of type 2 diabetes. However, the role and underlying mechanisms of IL-12 and the ER stress CHOP in endothelial dysfunction are not fully understood.
    Methods: We generated double knockout mice between db
    Results: The results showed that GTT was improved in db-/db
    Conclusion: Using a genetic approach, these findings provide evidence that IL-12 and ER stress CHOP play a significant role in microvascular endothelial dysfunction in type 2 diabetes.
    Language English
    Publishing date 2022-08-30
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2494854-8
    ISSN 1178-7007
    ISSN 1178-7007
    DOI 10.2147/DMSO.S369488
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Broken heart: A matter of the endoplasmic reticulum stress bad management?

    Belmadani, Souad / Matrougui, Khalid

    World journal of cardiology

    2019  Volume 11, Issue 6, Page(s) 159–170

    Abstract: Cardiovascular diseases are the number one cause of morbidity and mortality in the United States and worldwide. The induction of the endoplasmic reticulum (ER) stress, a result of a disruption in the ER homeostasis, was found to be highly associated with ...

    Abstract Cardiovascular diseases are the number one cause of morbidity and mortality in the United States and worldwide. The induction of the endoplasmic reticulum (ER) stress, a result of a disruption in the ER homeostasis, was found to be highly associated with cardiovascular diseases such as hypertension, diabetes, ischemic heart diseases and heart failure. This review will discuss the latest literature on the different aspects of the involvement of the ER stress in cardiovascular complications and the potential of targeting the ER stress pathways as a new therapeutic approach for cardiovascular complications.
    Language English
    Publishing date 2019-07-05
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2573665-6
    ISSN 1949-8462
    ISSN 1949-8462
    DOI 10.4330/wjc.v11.i6.159
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Letter by Belmadani et al Regarding Article, "Interleukin-35 Promotes Macrophage Survival and Improves Wound Healing After Myocardial Infarction in Mice".

    Belmadani, Souad / Frost, Michaela / Matrougui, Khalid

    Circulation research

    2020  Volume 126, Issue 4, Page(s) e10–e11

    MeSH term(s) Animals ; Interleukins ; Macrophages ; Mice ; Myocardial Infarction ; Wound Healing
    Chemical Substances Interleukins
    Language English
    Publishing date 2020-02-13
    Publishing country United States
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.119.316514
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui IV Zs.70: Show issues Location:
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  7. Article ; Online: The Unraveling Truth About IRE1 and MicroRNAs in Diabetes.

    Belmadani, Souad / Matrougui, Khalid

    Diabetes

    2017  Volume 66, Issue 1, Page(s) 23–24

    Language English
    Publishing date 2017-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/dbi16-0058
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Interleukin-1β Disruption Protects Male Mice From Heart Failure With Preserved Ejection Fraction Pathogenesis.

    Srinivas, Balaji K / Bourdi, Aya / O'Regan, Jacob D / Malavalli, Kumar D / Rhaleb, Nour-Eddine / Belmadani, Souad / Matrougui, Khalid

    Journal of the American Heart Association

    2023  Volume 12, Issue 14, Page(s) e029668

    Abstract: Background Heart failure with preserved ejection fraction (HFpEF) is a significant unmet need in cardiovascular medicine and remains an untreatable cardiovascular disease. The role and mechanism of interleukin-1β in HFpEF pathogenesis are poorly ... ...

    Abstract Background Heart failure with preserved ejection fraction (HFpEF) is a significant unmet need in cardiovascular medicine and remains an untreatable cardiovascular disease. The role and mechanism of interleukin-1β in HFpEF pathogenesis are poorly understood. Methods and Results C57/Bl6J and interleukin-1β
    MeSH term(s) Mice ; Male ; Animals ; Heart Failure/genetics ; Heart Failure/prevention & control ; Stroke Volume/physiology ; Interleukin-1beta ; Drinking Water ; Cardiomyopathies/complications ; Inflammation/pathology
    Chemical Substances Interleukin-1beta ; Drinking Water
    Language English
    Publishing date 2023-06-22
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.122.029668
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Diabetes and microvascular pathophysiology: role of epidermal growth factor receptor tyrosine kinase.

    Matrougui, Khalid

    Diabetes/metabolism research and reviews

    2009  Volume 26, Issue 1, Page(s) 13–16

    Abstract: Type 2 diabetes is responsible for the increased prevalence of ischaemic heart disease, generally related to coronary artery disease, which is associated with increased morbidity and death in diabetic patients. Epidermal growth factor receptor (EGFR) ... ...

    Abstract Type 2 diabetes is responsible for the increased prevalence of ischaemic heart disease, generally related to coronary artery disease, which is associated with increased morbidity and death in diabetic patients. Epidermal growth factor receptor (EGFR) tyrosine kinase, one of the many factors involved in cell growth and migration, has been shown to be key element in the development of microvessel myogenic tone. In a recent study, we have shown that microvascular dysfunction in type 2 diabetes is dependent on the exacerbation of the EGFR tyrosine kinase phosphorylation. Thus, further elucidation of this EGFR transactivation and down stream signalling will offer a new direction to investigate the mechanism of microvascular dysfunction responsible for heart disease that occurs in type 2 diabetes. In this review, we discuss the link between the EGFR transactivation and microvascular dysfunction that occurs in type 2 diabetes.
    MeSH term(s) Animals ; Diabetes Mellitus, Type 2/enzymology ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/pathology ; Diabetes Mellitus, Type 2/physiopathology ; Diabetic Angiopathies/enzymology ; Diabetic Angiopathies/genetics ; Diabetic Angiopathies/physiopathology ; Disease Models, Animal ; ErbB Receptors/genetics ; ErbB Receptors/physiology ; Humans ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Microcirculation/physiology
    Chemical Substances ErbB Receptors (EC 2.7.10.1) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
    Language English
    Publishing date 2009-11-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1470192-3
    ISSN 1520-7560 ; 1520-7552
    ISSN (online) 1520-7560
    ISSN 1520-7552
    DOI 10.1002/dmrr.1050
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  10. Article ; Online: Mitochondrial ATP6 and ND3 genes are associated with type 2 diabetic peripheral neuropathy.

    Kasinathan, Devi / Matrougui, Khalid / Elango, Santhini / Belmandani, Souad / Srinivas, Balaji / Muthusamy, Karthikeyan / Narayanasamy Marimuthu, Prabhu

    Diabetes & metabolic syndrome

    2022  Volume 16, Issue 6, Page(s) 102501

    Abstract: Background and aims: The association of mitochondrial NADH dehydrogenase gene mutations with type 2 diabetes in the Karaikudi population was previously reported. This is a case report that demonstrated rare mutations are responsible for maternally ... ...

    Abstract Background and aims: The association of mitochondrial NADH dehydrogenase gene mutations with type 2 diabetes in the Karaikudi population was previously reported. This is a case report that demonstrated rare mutations are responsible for maternally inherited peripheral neuropathy of diabetes.
    Methods: We describe a 70-year-old male and his family (n = 25) with type 2 diabetic peripheral neuropathy having four rare mutations, 8597T > C, 8699T > C, 8966T > C, 10188A > G, and 9 bp deletion in various regions of the mitochondrial genes. Mutations were identified through direct sequencing of DNA isolated from the blood of the selected individuals. Blood samples were also analyzed for glucose, hemoglobin A1c, triglyceride, total cholesterol, oxidative stress markers, antioxidant status, cytochrome-C-oxidase and mitochondrial DNA content using appropriate methods.
    Results: Oxidative stress markers were found elevated while the antioxidant status, mitochondrial DNA content and the activity of cytochrome C-oxidase was reduced significantly. Analysis of mtDNA showed the presence of several mutations in various regions of mitochondrial genome. However, 8597T > C, 8699T > C, 8966T > C, 10188A > G, and 9 bp deletion were observed in the patient's family including his siblings.
    Conclusion: This study shows that the mutations observed in the patient and his family is maternally inherited and suspected to be pathogenic in developing T2D associated peripheral neuropathy.
    MeSH term(s) Aged ; Antioxidants ; DNA, Mitochondrial/genetics ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/genetics ; Diabetic Neuropathies/genetics ; Humans ; Male ; Mutation ; Oxidoreductases/genetics
    Chemical Substances Antioxidants ; DNA, Mitochondrial ; Oxidoreductases (EC 1.-)
    Language English
    Publishing date 2022-05-16
    Publishing country Netherlands
    Document type Case Reports
    ZDB-ID 2273766-2
    ISSN 1878-0334 ; 1871-4021
    ISSN (online) 1878-0334
    ISSN 1871-4021
    DOI 10.1016/j.dsx.2022.102501
    Database MEDical Literature Analysis and Retrieval System OnLINE

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