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  1. Article ; Online: Editorial: Special issue: Non-alcoholic fatty liver disease: From molecular basis to therapeutic advances.

    Nasiri-Ansari, Narjes / Kassi, Eva

    Metabolism open

    2023  Volume 17, Page(s) 100229

    Language English
    Publishing date 2023-01-13
    Publishing country England
    Document type Editorial
    ISSN 2589-9368
    ISSN (online) 2589-9368
    DOI 10.1016/j.metop.2023.100229
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  2. Article ; Online: Defective Anti-oxidant System: An Aggravating Factor for COVID-19 Patients Outcome?

    Kassi, Eva N / Papavassiliou, Kostas A / Papavassiliou, Athanasios G

    Archives of medical research

    2020  Volume 51, Issue 7, Page(s) 726–727

    MeSH term(s) Antioxidants/metabolism ; COVID-19/physiopathology ; COVID-19/therapy ; Humans ; Oxidative Stress ; SARS-CoV-2
    Chemical Substances Antioxidants
    Keywords covid19
    Language English
    Publishing date 2020-05-22
    Publishing country United States
    Document type Letter
    ZDB-ID 1156844-6
    ISSN 1873-5487 ; 0188-4409 ; 0188-0128
    ISSN (online) 1873-5487
    ISSN 0188-4409 ; 0188-0128
    DOI 10.1016/j.arcmed.2020.05.017
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  3. Article ; Online: G6PD and chloroquine: Selecting the treatment against SARS-CoV-2?

    Kassi, Eva N / Papavassiliou, Kostas A / Papavassiliou, Athanasios G

    Journal of cellular and molecular medicine

    2020  Volume 24, Issue 9, Page(s) 4913–4914

    MeSH term(s) Betacoronavirus/physiology ; Chloroquine/adverse effects ; Coronavirus Infections/drug therapy ; Glucosephosphate Dehydrogenase/metabolism ; Glucosephosphate Dehydrogenase Deficiency/complications ; Humans
    Chemical Substances Chloroquine (886U3H6UFF) ; Glucosephosphate Dehydrogenase (EC 1.1.1.49)
    Keywords covid19
    Language English
    Publishing date 2020-04-16
    Publishing country England
    Document type Editorial
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.15312
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    Zs.A 5752: Show issues Location:
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  4. Article ; Online: Structural Speciation of Ti(IV)-(α-Hydroxycarboxylic Acid) Complexes in Metabolism-Related (Patho)Physiology-In Vitro Approaches to (Pre)Adipocyte Differentiation and Mineralization.

    Tsave, Olga / Iordanidou, Catherine / Hatzidimitriou, Antonios / Yavropoulou, Maria P / Kassi, Eva N / Nasiri-Ansari, Narjes / Gabriel, Catherine / Salifoglou, Athanasios

    International journal of molecular sciences

    2023  Volume 24, Issue 14

    Abstract: The prospect of developing soluble and bioavailable Ti(IV) complex forms with physiological substrates, capable of influencing (patho)physiological aberrations, emerges as a challenge in the case of metabolism-related pathologies (e.g., diabetes mellitus ...

    Abstract The prospect of developing soluble and bioavailable Ti(IV) complex forms with physiological substrates, capable of influencing (patho)physiological aberrations, emerges as a challenge in the case of metabolism-related pathologies (e.g., diabetes mellitus 1 and 2). To that end, pH-specific synthetic efforts on binary Ti(IV)-(α-hydroxycarboxylic acid) systems, involving natural physiological chelator ligands (α-hydroxy isobutyric acid, D-quinic acid, 2-ethyl-2-hydroxybutyric acid) in aqueous media, led to the successful isolation of binary crystalline Ti(IV)-containing products. The new materials were physicochemically characterized by elemental analysis, FT-IR, TGA, and X-ray crystallography, revealing in all cases the presence of mononuclear Ti(IV) complexes bearing a TiO
    MeSH term(s) Ligands ; Titanium/pharmacology ; Titanium/chemistry ; Spectroscopy, Fourier Transform Infrared ; Cell Differentiation ; Carboxylic Acids/chemistry ; Adipocytes ; Crystallography, X-Ray
    Chemical Substances Ligands ; Titanium (D1JT611TNE) ; Carboxylic Acids
    Language English
    Publishing date 2023-07-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241411865
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  7. Article ; Online: Defective Anti-oxidant System

    Kassi, Eva N. / Papavassiliou, Kostas A. / Papavassiliou, Athanasios G.

    Archives of Medical Research

    An Aggravating Factor for COVID-19 Patients Outcome?

    2020  Volume 51, Issue 7, Page(s) 726–727

    Keywords General Medicine ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 1156844-6
    ISSN 0188-4409 ; 0188-0128
    ISSN 0188-4409 ; 0188-0128
    DOI 10.1016/j.arcmed.2020.05.017
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  8. Article ; Online: G6PD and chloroquine

    Kassi, Eva N. / Papavassiliou, Kostas A. / Papavassiliou, Athanasios G.

    Journal of Cellular and Molecular Medicine

    Selecting the treatment against SARS‐CoV‐2?

    2020  Volume 24, Issue 9, Page(s) 4913–4914

    Keywords Molecular Medicine ; Cell Biology ; covid19
    Language English
    Publisher Wiley
    Publishing country us
    Document type Article ; Online
    ZDB-ID 2074559-X
    ISSN 1582-4934 ; 1582-4934 ; 1582-1838
    ISSN (online) 1582-4934
    ISSN 1582-4934 ; 1582-1838
    DOI 10.1111/jcmm.15312
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  9. Article ; Online: Atherosclerotic and Cardio-Metabolic Diseases

    Eva Kassi / Ioannis Kyrou / Harpal S. Randeva

    International Journal of Molecular Sciences, Vol 24, Iss 9737, p

    From Molecular Basis to Therapeutic Advances

    2023  Volume 9737

    Abstract: Cardiovascular diseases (CVDs) still remain the major cause of death worldwide; however, CVD-related mortality has been reduced due to lifestyle modification interventions, as well as novel pharmacological therapies and advances in cardiovascular surgery ...

    Abstract Cardiovascular diseases (CVDs) still remain the major cause of death worldwide; however, CVD-related mortality has been reduced due to lifestyle modification interventions, as well as novel pharmacological therapies and advances in cardiovascular surgery [.]
    Keywords n/a ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Language English
    Publishing date 2023-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
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  10. Article ; Online: Endoplasmic reticulum stress in nonalcoholic (metabolic associated) fatty liver disease (NAFLD/MAFLD).

    Flessa, Christina-Maria / Kyrou, Ioannis / Nasiri-Ansari, Narjes / Kaltsas, Gregory / Kassi, Eva / Randeva, Harpal S

    Journal of cellular biochemistry

    2022  Volume 123, Issue 10, Page(s) 1585–1606

    Abstract: Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic fat accumulation in the absence of excessive alcohol consumption and is strongly associated with obesity, type 2 diabetes (T2DM) and other metabolic syndrome features. NAFLD is becoming ...

    Abstract Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic fat accumulation in the absence of excessive alcohol consumption and is strongly associated with obesity, type 2 diabetes (T2DM) and other metabolic syndrome features. NAFLD is becoming increasingly prevalent and currently constitutes the leading cause of hepatocellular carcinoma (HCC). Recently, the term metabolic (dysfunction) associated fatty liver disease (MAFLD) has been proposed reflecting more accurately the underlying pathogenesis and the cardiometabolic disorders associated to NAFLD/MAFLD. Given the vital metabolic functions of the liver to maintain the body homeostasis, an extended endoplasmic reticulum (ER) network is mandatory in hepatocytes to retain its capacity to adapt to the multiple extracellular and intracellular signals mediating metabolic changes. Dysfunction of hepatocyte ER homeostasis and disturbance of its interaction with mitochondria have been recognized to be involved in the NAFLD pathophysiology. Apart from hepatocytes, hepatic stellate cells, and Kupffer cells have been shown to play an important role in the occurrence of NAFLD and progression to nonalcoholic steatohepatitis (NASH) with possibly different roles in the different stages of the NAFLD spectrum. Furthermore, excess lipid accumulation in the liver causes lipotoxicity which interacts with ER stress and culminates in inflammation and hepatocellular damage, mechanisms crucially implicated in NASH pathogenesis. Finally, the circadian clock machinery regulates ER stress-related pathways and vice versa, thus controlling the homeostasis of the liver metabolism and being implicated in the NAFLD progression. This review presents a comprehensive overview of the current knowledge supporting the impact of ER stress signaling on NAFLD, whilst summarizing potential therapeutic interventions targeting this process.
    MeSH term(s) Humans ; Non-alcoholic Fatty Liver Disease/metabolism ; Endoplasmic Reticulum Stress ; Carcinoma, Hepatocellular/pathology ; Diabetes Mellitus, Type 2/metabolism ; Liver Neoplasms/pathology ; Liver/metabolism
    Language English
    Publishing date 2022-05-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.30247
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