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  1. Article ; Online: Incorporating functional genomics into the pathology-supported genetic testing framework implemented in South Africa: A future view of precision medicine for breast carcinomas.

    Christowitz, Claudia / Olivier, Daniel W / Schneider, Johann W / Kotze, Maritha J / Engelbrecht, Anna-Mart

    Mutation research. Reviews in mutation research

    2024  Volume 793, Page(s) 108492

    Abstract: A pathology-supported genetic testing (PSGT) framework was established in South Africa to improve access to precision medicine for patients with breast carcinomas. Nevertheless, the frequent identification of variants of uncertain significance (VUSs) ... ...

    Abstract A pathology-supported genetic testing (PSGT) framework was established in South Africa to improve access to precision medicine for patients with breast carcinomas. Nevertheless, the frequent identification of variants of uncertain significance (VUSs) with the use of genome-scale next-generation sequencing has created a bottleneck in the return of results to patients. This review highlights the importance of incorporating functional genomics into the PSGT framework as a proposed initiative. Here, we explore various model systems and experimental methods available for conducting functional studies in South Africa to enhance both variant classification and clinical interpretation. We emphasize the distinct advantages of using in vitro, in vivo, and translational ex vivo models to improve the effectiveness of precision oncology. Moreover, we highlight the relevance of methodologies such as protein modelling and structural bioinformatics, multi-omics, metabolic activity assays, flow cytometry, cell migration and invasion assays, tube-formation assays, multiplex assays of variant effect, and database mining and machine learning models. The selection of the appropriate experimental approach largely depends on the molecular mechanism of the gene under investigation and the predicted functional effect of the VUS. However, before making final decisions regarding the pathogenicity of VUSs, it is essential to assess the functional evidence and clinical outcomes under current variant interpretation guidelines. The inclusion of a functional genomics infrastructure within the PSGT framework will significantly advance the reclassification of VUSs and enhance the precision medicine pipeline for patients with breast carcinomas in South Africa.
    Language English
    Publishing date 2024-04-15
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 2727833-5
    ISSN 1388-2139 ; 1383-5742
    ISSN (online) 1388-2139
    ISSN 1383-5742
    DOI 10.1016/j.mrrev.2024.108492
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The impact of endocrine disrupting compounds and carcinogens in wastewater: Implications for breast cancer.

    du Plessis, Manisha / Fourie, Carla / Stone, Wendy / Engelbrecht, Anna-Mart

    Biochimie

    2023  Volume 209, Page(s) 103–115

    Abstract: The incidence of breast cancer is often associated with geographic variation which indicates that a person's surrounding environment can be an important etiological factor in cancer development. Environmental risk factors can include exposure to sewage- ... ...

    Abstract The incidence of breast cancer is often associated with geographic variation which indicates that a person's surrounding environment can be an important etiological factor in cancer development. Environmental risk factors can include exposure to sewage- or wastewater, which consist of a complex mixture of pathogens, mutagens and carcinogens. Wastewater contains primarily carbonaceous, nitrogenous and phosphorus compounds, however it can also contain trace amounts of chemical pollutants including toxic metal cations, hydrocarbons and pesticides. More importantly, the contamination of drinking water by wastewater is a potential source of exposure to mammary carcinogens and endocrine disrupting compounds. Organic solvents and other pollutants often found in wastewater have been detected in various tissues, including breast and adipose tissues. Furthermore, these pollutants such as phenolic compounds in some detergents and plastics, as well as parabens and pesticides can mimic estrogen. High estrogen levels are a well-established risk factor for estrogen-receptor (ER) positive breast cancer. Therefore, exposure to wastewater is a risk factor for the initiation, progression and metastasis of breast cancer. Carcinogens present in wastewater can promote tumourigenesis through various mechanisms, including the formation of DNA adducts, gene mutations and oxidative stress. Lastly, the presence of endocrine disrupting compounds in wastewater can have negative implications for ER-positive breast cancers, where these molecules can activate ERα to promote cell proliferation, survival and metastasis. As such, strategies should be implemented to limit exposure, such as providing funding into treatment technologies and implementation of regulations that limit the production and use of these potentially harmful chemicals.
    MeSH term(s) Humans ; Female ; Breast Neoplasms/chemically induced ; Breast Neoplasms/epidemiology ; Carcinogens/toxicity ; Wastewater/toxicity ; Estrogens ; Environmental Pollutants ; Pesticides/toxicity ; Endocrine Disruptors/toxicity ; Endocrine Disruptors/analysis
    Chemical Substances Carcinogens ; Wastewater ; Estrogens ; Environmental Pollutants ; Pesticides ; Endocrine Disruptors
    Language English
    Publishing date 2023-02-11
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 120345-9
    ISSN 1638-6183 ; 0300-9084
    ISSN (online) 1638-6183
    ISSN 0300-9084
    DOI 10.1016/j.biochi.2023.02.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The impact of endocrine disrupting compounds and carcinogens in wastewater: Implications for breast cancer

    du Plessis, Manisha / Fourie, Carla / Stone, Wendy / Engelbrecht, Anna-Mart

    Biochimie. 2023 June, v. 209 p.103-115

    2023  

    Abstract: The incidence of breast cancer is often associated with geographic variation which indicates that a person's surrounding environment can be an important etiological factor in cancer development. Environmental risk factors can include exposure to sewage- ... ...

    Abstract The incidence of breast cancer is often associated with geographic variation which indicates that a person's surrounding environment can be an important etiological factor in cancer development. Environmental risk factors can include exposure to sewage- or wastewater, which consist of a complex mixture of pathogens, mutagens and carcinogens. Wastewater contains primarily carbonaceous, nitrogenous and phosphorus compounds, however it can also contain trace amounts of chemical pollutants including toxic metal cations, hydrocarbons and pesticides. More importantly, the contamination of drinking water by wastewater is a potential source of exposure to mammary carcinogens and endocrine disrupting compounds. Organic solvents and other pollutants often found in wastewater have been detected in various tissues, including breast and adipose tissues. Furthermore, these pollutants such as phenolic compounds in some detergents and plastics, as well as parabens and pesticides can mimic estrogen. High estrogen levels are a well-established risk factor for estrogen-receptor (ER) positive breast cancer. Therefore, exposure to wastewater is a risk factor for the initiation, progression and metastasis of breast cancer. Carcinogens present in wastewater can promote tumourigenesis through various mechanisms, including the formation of DNA adducts, gene mutations and oxidative stress. Lastly, the presence of endocrine disrupting compounds in wastewater can have negative implications for ER-positive breast cancers, where these molecules can activate ERα to promote cell proliferation, survival and metastasis. As such, strategies should be implemented to limit exposure, such as providing funding into treatment technologies and implementation of regulations that limit the production and use of these potentially harmful chemicals.
    Keywords DNA adducts ; breast neoplasms ; breasts ; carcinogenesis ; cell proliferation ; estrogens ; etiology ; genes ; geographical variation ; metastasis ; oxidative stress ; phosphorus ; risk factors ; toxicity ; wastewater ; Estrogen ; Carcinogen ; Endocrine disruptors ; Breast cancer
    Language English
    Dates of publication 2023-06
    Size p. 103-115.
    Publishing place Elsevier B.V.
    Document type Article ; Online
    ZDB-ID 120345-9
    ISSN 0300-9084
    ISSN 0300-9084
    DOI 10.1016/j.biochi.2023.02.006
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: To clot, or not to clot: The dilemma of hormone treatment options for menopause.

    Booyens, Renata M / Engelbrecht, Anna-Mart / Strauss, Ledivia / Pretorius, Etheresia

    Thrombosis research

    2022  Volume 218, Page(s) 99–111

    Abstract: Untreated menopause may have serious health implications, but treatments can have dangerous side effects. We evaluate menopausal symptoms as well as available treatments -the routes of administration and their effect on blood coagulation. Menopausal ... ...

    Abstract Untreated menopause may have serious health implications, but treatments can have dangerous side effects. We evaluate menopausal symptoms as well as available treatments -the routes of administration and their effect on blood coagulation. Menopausal females may experience hot flushes, vulva- and vaginal atrophy and osteoporosis. Many treatments are available to relieve these symptoms such as Conjugated Equine Estrogen and bioidentical hormones. The routes of administration include oral and transdermal. Hormones that are administered orally undergo a hepatic first pass metabolism. The by-products have a lower efficacy and possibly enhanced side effects. Furthermore, hormone treatments influence the coagulation cascade through coagulation factors or their regulators. Increased coagulation poses a risk for venous thromboembolism. Currently a definite conclusion on whether the side effects from hormone treatments exceed the risk of untreated menopause cannot be made. However, a more individualised approach to hormone treatments may be the most feasible solution to this dilemma.
    MeSH term(s) Estradiol ; Estrogen Replacement Therapy/adverse effects ; Estrogens/therapeutic use ; Estrogens, Conjugated (USP)/adverse effects ; Estrogens, Conjugated (USP)/therapeutic use ; Female ; Hot Flashes/chemically induced ; Hot Flashes/drug therapy ; Humans ; Menopause ; Thrombosis/etiology
    Chemical Substances Estrogens ; Estrogens, Conjugated (USP) ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2022-08-19
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 121852-9
    ISSN 1879-2472 ; 0049-3848
    ISSN (online) 1879-2472
    ISSN 0049-3848
    DOI 10.1016/j.thromres.2022.08.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Obese mammary tumour-bearing mice are highly sensitive to doxorubicin-induced hepatotoxicity.

    Sedeman, Megan / Christowitz, Claudia / de Jager, Louis / Engelbrecht, Anna-Mart

    BMC cancer

    2022  Volume 22, Issue 1, Page(s) 1240

    Abstract: Background: Breast cancer is a major health burden for women, worldwide. Lifestyle-related risk factors, such as obesity and being overweight, have reached epidemic proportions and contributes to the development of breast cancer. Doxorubicin (DXR) is a ... ...

    Abstract Background: Breast cancer is a major health burden for women, worldwide. Lifestyle-related risk factors, such as obesity and being overweight, have reached epidemic proportions and contributes to the development of breast cancer. Doxorubicin (DXR) is a chemotherapeutic drug commonly used to treat breast cancer, and although effective, may cause toxicity to other organs. The mechanisms and effects of DXR on hepatic tissue, and the contributing role of obesity, in breast cancer patients are poorly understood. The aim of this study was therefore to investigate the effects of DXR on hepatic tissue in an obese tumour-bearing mouse model.
    Methods: A diet-induced obesity (DIO) mouse model was established, where seventy-four three-week-old female C57BL6 mice were divided into two main groups, namely the high fat diet (containing 60% kcal fat) and standard diet (containing 10% kcal fat) groups. After eight weeks on their respective diets, the DIO phenotype was established, and the mice were further divided into tumour and non-tumour groups. Mice were subcutaneously inoculated with E0771 triple negative breast cancer cells in the fourth mammary gland and received three doses of 4 mg/kg DXR (cumulative dosage of 12 mg/kg) or vehicle treatments via intraperitoneal injection. The expression levels of markers involved in apoptosis and alanine aminotransferase (ALT) were compared by means of western blotting. To assess the pathology and morphology of hepatic tissue, haematoxylin and eosin staining was performed. The presence of fibrosis and lipid accumulation in hepatic tissues were assessed with Masson's trichrome and Oil Red O staining, respectively.
    Results: Microscopic examination of liver tissues showed significant changes in the high fat diet tumour-bearing mice treated with DXR, consisting of macrovesicular steatosis, hepatocyte ballooning and lobular inflammation, compared to the standard diet tumour-bearing mice treated with DXR and the control group (standard diet mice). These changes are the hallmarks of non-alcoholic fatty liver disease, associated with obesity.
    Conclusion: The histopathological findings indicated that DXR caused significant hepatic parenchymal injury in the obese tumour-bearing mice. Hepatotoxicity is aggravated in obesity as an underlying co-morbidity. It has been shown that obesity is associated with poor clinical outcomes in patients receiving neo-adjuvant chemotherapy treatment regimens.
    MeSH term(s) Female ; Animals ; Mice ; Mice, Obese ; Mice, Inbred C57BL ; Mammary Neoplasms, Animal ; Doxorubicin/adverse effects ; Obesity/complications ; Disease Models, Animal ; Chemical and Drug Induced Liver Injury
    Chemical Substances Doxorubicin (80168379AG)
    Language English
    Publishing date 2022-11-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041352-X
    ISSN 1471-2407 ; 1471-2407
    ISSN (online) 1471-2407
    ISSN 1471-2407
    DOI 10.1186/s12885-022-10189-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The effect of HIF-1α inhibition in breast cancer cells prior to doxorubicin treatment under conditions of normoxia and hypoxia.

    Fourie, Carla / du Plessis, Manisha / Mills, Justin / Engelbrecht, Anna-Mart

    Experimental cell research

    2022  Volume 419, Issue 2, Page(s) 113334

    Abstract: Background: Oxygen deprivation is a key hallmark within solid tumours that contributes to breast-tumour pathophysiology. Under these conditions, neoplastic cells activate several genes, regulated by the HIF-1 transcription factor, which alters the ... ...

    Abstract Background: Oxygen deprivation is a key hallmark within solid tumours that contributes to breast-tumour pathophysiology. Under these conditions, neoplastic cells activate several genes, regulated by the HIF-1 transcription factor, which alters the tumour microenvironment to promote survival - including resistance to cell death in therapeutic attempts such as doxorubicin (Dox) treatment.
    Methods: We investigated HIF-1ɑ as a therapeutic target to sensitize breast cancer cells to Dox treatment. Under both normoxic (21% O
    Results: Here we observed that an inverse relationship between HIF-1ɑ and apoptosis exists and that Dox promotes autophagy under hypoxic conditions. Although adjuvant therapy with 2-ME induced an antagonistic effect in breast cancer cells, upregulated HIF-1ɑ expression in a hypoxic environment promotes treatment resistance and this was attenuated once HIF-1ɑ gene expression was silenced.
    Conclusion: Therefore, highlighting the identification of possible hypoxia-targeting therapies for breast cancer patients can be beneficial by promoting more favourable treatment responses.
    MeSH term(s) Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Hypoxia ; Cell Line, Tumor ; Doxorubicin/pharmacology ; Female ; Humans ; Hypoxia ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; MCF-7 Cells ; Mercaptoethanol/pharmacology ; Tumor Microenvironment
    Chemical Substances Hypoxia-Inducible Factor 1, alpha Subunit ; Mercaptoethanol (60-24-2) ; Doxorubicin (80168379AG)
    Language English
    Publishing date 2022-08-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2022.113334
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Insulin-mediated immune dysfunction in the development of preeclampsia.

    van Niekerk, Gustav / Christowitz, Claudia / Engelbrecht, Anna-Mart

    Journal of molecular medicine (Berlin, Germany)

    2021  Volume 99, Issue 7, Page(s) 889–897

    Abstract: Epidemiological observations implicate insulin resistance as a predisposing factor in the development of preeclampsia (PE). It is also well established that PE manifests in the context of a dysregulated immune response at the maternal-foetal interface, ... ...

    Abstract Epidemiological observations implicate insulin resistance as a predisposing factor in the development of preeclampsia (PE). It is also well established that PE manifests in the context of a dysregulated immune response at the maternal-foetal interface, though all the underlying drivers of such immune dysregulation remains to be accounted for. Although it has long been known that various immune cells express insulin receptors following immune activation, it is only recently that insulin signalling has been shown to play a key role in immune cell differentiation, survival and effector function through its canonical activation of the PI3K/Akt/mTOR pathway. Here we argue that hyperinsulinemia, manifesting either from insulin resistance or from intensive insulin therapy, likely plays a direct role in driving immune cell dysfunction which plays a central role in the development of PE. This line of reasoning also explains the superior results of insulin-sparing interventions compared to intensive insulin therapy as monotherapy.
    MeSH term(s) Animals ; Female ; Humans ; Hyperglycemia/immunology ; Inflammation/immunology ; Insulin/immunology ; Insulin Resistance ; Pre-Eclampsia/immunology ; Pregnancy
    Chemical Substances Insulin
    Language English
    Publishing date 2021-03-25
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1223802-8
    ISSN 1432-1440 ; 0946-2716
    ISSN (online) 1432-1440
    ISSN 0946-2716
    DOI 10.1007/s00109-021-02068-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Serum amyloid A1: Innocent bystander or active participant in cell migration in triple-negative breast cancer?

    Olivier, Daniel Wilhelm / Pretorius, Etheresia / Engelbrecht, Anna-Mart

    Experimental cell research

    2021  Volume 406, Issue 1, Page(s) 112759

    Abstract: The Serum Amyloid A (SAA) family of proteins is associated with various pathological conditions, including cancer. However, their role in cancer is incompletely understood. Here, we investigated the role of SAA1 in cell cycle regulation, apoptosis, ... ...

    Abstract The Serum Amyloid A (SAA) family of proteins is associated with various pathological conditions, including cancer. However, their role in cancer is incompletely understood. Here, we investigated the role of SAA1 in cell cycle regulation, apoptosis, survival signaling, metabolism, and metastasis in models of triple-negative breast cancer (TNBC), using RNAi. Our data show that in untransformed epithelial cells (MCF12A), the knockdown of SAA1 induces the expression of cell cycle regulators (MCM2, p53), the activation of DNA repair (PARP synthesis), and survival signaling (NFκB). In contrast, knockdown of SAA1 in the TNBC cell line (MDA-MB-231) induced the expression p16 and shifted cells in the cell cycle from the S to G
    MeSH term(s) Actins/genetics ; Actins/metabolism ; Antigens, CD/genetics ; Antigens, CD/metabolism ; Apoptosis/genetics ; Cadherins/genetics ; Cadherins/metabolism ; Cell Cycle/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Epithelial-Mesenchymal Transition ; Gene Expression Regulation, Neoplastic ; Humans ; Laminin/genetics ; Laminin/metabolism ; Minichromosome Maintenance Complex Component 2/genetics ; Minichromosome Maintenance Complex Component 2/metabolism ; Models, Biological ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Poly(ADP-ribose) Polymerases/genetics ; Poly(ADP-ribose) Polymerases/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Serum Amyloid A Protein/antagonists & inhibitors ; Serum Amyloid A Protein/genetics ; Serum Amyloid A Protein/metabolism ; Signal Transduction ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/metabolism ; Triple Negative Breast Neoplasms/pathology ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Vimentin/genetics ; Vimentin/metabolism
    Chemical Substances ACTA2 protein, human ; Actins ; Antigens, CD ; CDH1 protein, human ; Cadherins ; Cyclin-Dependent Kinase Inhibitor p16 ; Laminin ; NF-kappa B ; RNA, Small Interfering ; SAA1 protein, human ; Serum Amyloid A Protein ; Tumor Suppressor Protein p53 ; VIM protein, human ; Vimentin ; laminin 1 ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30) ; MCM2 protein, human (EC 3.6.4.12) ; Minichromosome Maintenance Complex Component 2 (EC 3.6.4.12)
    Language English
    Publishing date 2021-07-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2021.112759
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Nutritional support in sepsis: when less may be more.

    van Niekerk, Gustav / Meaker, Charné / Engelbrecht, Anna-Mart

    Critical care (London, England)

    2020  Volume 24, Issue 1, Page(s) 53

    Abstract: Despite sound basis to suspect that aggressive and early administration of nutritional support may hold therapeutic benefits during sepsis, recommendations for nutritional support have been somewhat underwhelming. Current guidelines (ESPEN and ASPEN) ... ...

    Abstract Despite sound basis to suspect that aggressive and early administration of nutritional support may hold therapeutic benefits during sepsis, recommendations for nutritional support have been somewhat underwhelming. Current guidelines (ESPEN and ASPEN) recognise a lack of clear evidence demonstrating the beneficial effect of nutritional support during sepsis, raising the question: why, given the perceived low efficacy of nutritionals support, are there no high-quality clinical trials on the efficacy of permissive underfeeding in sepsis? Here, we review clinically relevant beneficial effects of permissive underfeeding, motivating the urgent need to investigate the clinical benefits of delaying nutritional support during sepsis.
    MeSH term(s) Critical Illness ; Energy Intake ; Enteral Nutrition ; Humans ; Nutritional Requirements ; Nutritional Support ; Sepsis
    Language English
    Publishing date 2020-02-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2041406-7
    ISSN 1466-609X ; 1364-8535
    ISSN (online) 1466-609X
    ISSN 1364-8535
    DOI 10.1186/s13054-020-2771-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Diabetes and susceptibility to infections: Implication for COVID-19.

    van Niekerk, Gustav / van der Merwe, Michelle / Engelbrecht, Anna-Mart

    Immunology

    2021  Volume 164, Issue 3, Page(s) 467–475

    Abstract: A number of mechanisms have been proposed to explain the well-established link between diabetic status and an increased susceptibility to infection. Notably, diabetes has been shown to be one of the strongest factors influencing healthcare outcome in ... ...

    Abstract A number of mechanisms have been proposed to explain the well-established link between diabetic status and an increased susceptibility to infection. Notably, diabetes has been shown to be one of the strongest factors influencing healthcare outcome in COVID-19 infections. Though it has long been noted that lymphocytes upregulate insulin receptors following immune activation, until recently, this observation has received little attention. Here, we point out key findings implicating dysregulated insulin signalling in immune cells as a possible contributing factor in the immune pathology associated with diabetes. Mechanistically, insulin, by activating the PI3K/Akt/mTOR pathway, regulates various aspects of both myeloid cells and lymphocytes, such as cell survival, metabolic reprogramming and the polarization and differentiation of immune cells. PI3K signalling is also supressed by immune checkpoint proteins, suggesting that insulin signalling may antagonize peripheral tolerance. Remarkably, it has also recently been shown that, following insulin binding, the insulin receptor translocates to the nucleus where it plays a key role in regulating the transcription of various immune-related genes, including pathways involved in viral infections. Taken together, these observations suggest that dysregulated insulin signalling may directly contribute to a defective immune response during COVID-19 infections.
    MeSH term(s) Animals ; Biomarkers/blood ; Blood Glucose/metabolism ; COVID-19/immunology ; COVID-19/metabolism ; COVID-19/physiopathology ; COVID-19/virology ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/physiopathology ; Host-Pathogen Interactions ; Humans ; Immune Checkpoint Proteins/metabolism ; Insulin/metabolism ; Insulin Resistance ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Lymphocytes/virology ; Phosphatidylinositol 3-Kinase/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Receptor, Insulin/metabolism ; SARS-CoV-2/immunology ; SARS-CoV-2/metabolism ; SARS-CoV-2/pathogenicity ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Biomarkers ; Blood Glucose ; Immune Checkpoint Proteins ; Insulin ; MTOR protein, human (EC 2.7.1.1) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Receptor, Insulin (EC 2.7.10.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2021-06-24
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/imm.13383
    Database MEDical Literature Analysis and Retrieval System OnLINE

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