Publications by authors named "Basheer Abdullah Marzoog"

Since coronavirus disease infection-19 (COVID-19) entry to the cells is angiotensin enzyme receptor (ACEII) dependent, extrapulmonary manifestations have been suspected. Ocular manifestations reported in several studies to involve the anterior as well as posterior eye segments. However, the predominance of the anterior eye segment reduced the attention of the scientific community on the posterior eye segment.

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Ischemic heart disease (IHD) is a pathology of global interest because it is widespread and has high morbidity and mortality. IHD pathophysiology involves local and systemic changes, including lipidomic, proteomic, and inflammasome changes in serum plasma. The modulation in these metabolites is viable in the pre-IHD, during the IHD period, and after management of IHD in all forms, including lifestyle changes and pharmacological and surgical interventions.

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Developing a novel risk score for accurate assessment of cardiovascular disease (CVD) morbidity and mortality is an urgent need in terms of early prevention and diagnosis and, thereafter, management, particularly of ischemic heart disease. The currently used scores for the evaluation of cardiovascular disease based on the classical risk factors suffer from severe limitations, including inaccurate predictive values. Therefore, we suggest adding a novel non-classical risk factor, including the level of specific exhaled volatile organic compounds that are associated with ischemic heart disease, to the SCORE2 and SCORE2-OP algorithms.

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Coronavirus infection disease-19 (COVID-19) is a worldwide catastrophic emergency that first appeared in late 2019, in Wuhan, China. COVID-19 is a multitropism disease that first affects lung tissue. However, extrapulmonary manifestations have been suspected from the first COVID-19 cases.

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Transcription factors play a crucial role in providing identity to each cell population. To maintain cell identity, it is essential to balance the expression of activator and inhibitor transcription factors. Cell plasticity and reprogramming offer great potential for future therapeutic applications, as they can regenerate damaged tissue.

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Background: Post-myocardial infarction (MI) changes have been frequently reported in the literature and are associated with determining the prognosis.

Aims: The aim of this study is to find a prognosis marker for the favorability of determination of the medium-term outcomes in patients with acute MI.

Objectives: MI patients' prognosis is poorly understood and requires further elaboration.

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Background: Numerous complications, such as postoperative arrhythmia and stroke, have been observed following coronary artery bypass graft (CABG) surgery.

Aims: This study sought to examine the impact of aging on the incidence of post-coronary artery shunt complications.

Objectives: Aging is a physiological process experienced by every living cell, beginning early in development.

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Entropy is a natural process that affects all living cells, including senescence, an irreversible physiological process that impairs cell homeostasis. Age is a significant factor in disease development, and the pathogenesis of endothelial cell aging is multifactorial. Autophagy dysfunction accelerates endothelial cell aging and cell death, while autophagy preserves endothelial cell youthfulness through intracellular homeostasis and gene expression regulation.

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Physiologically, cytokines play an extremely important role in maintaining cellular and subcellular homeostasis, as they interact almost with every cell in the organism. Therefore, cytokines play a significantly critical role in the field of pathogenic pharmacological therapy of different types of pathologies. Cytokine is a large family containing many subfamilies and can be evaluated into groups according to their action on epithelial cell proliferation; stimulatory include transforming growth factor-α (TGF-α), Interlukine-22 (IL-22), IL-13, IL-6, IL-1RA and IL-17 and inhibitory include IL-1α, interferon type I (IFN type I), and TGF-β.

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Cellular and subcellular metabolic activities are crucial processes involved in the regulation of intracellular homeostasis, including cellular and subcellular signaling pathways. Dysregulation of intracellular regulation mechanisms is catastrophic and cumulates into cell death. To overcome the issue of dysregulation of intracellular regulation mechanisms, the preservation of subcellular and extracellular components is essential to maintain healthy cells with increased longevity.

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Background: Cardiovascular disease and diabetes mellitus are among the leading causes of mortality.

Objectives: Our study evaluated endothelial function in patients with arterial hypertension, coronary heart disease, and diabetes mellitus.

Aims: This study aimed to assess the degree of endothelial dysfunction in individuals with cardiovascular risk factors older than 55 years of age.

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Autophagy plays a crucial role in maintaining endothelial cell homeostasis through the turnover of intracellular components during stress conditions in a lysosomal-dependent manner. The regeneration strategy involves several aspects, including autophagy. Autophagy is a catabolic degenerative lysosomal-dependent degradation of intracellular components.

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COVID-19 is a global health emergency that requires worldwide collaboration to control its spread. The scientific community is working to understand the different aspects of the post-COVID-19 syndrome and potential treatment strategies. Interestingly, there have been reports of gastrointestinal tract (GIT) involvement in the post-COVID-19 syndrome, suggesting the presence of both severe and mild GIT disorders.

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Hypothermia and autophagy are critical regulators of cell homeostasis by regulating intra and intercellular cell communication. Myocardiocyte cryotherapy poses multiple cellular and subcellular effects on the injured cell, including upregulation of autophagy. Autophagy plays a crucial role in modifying cell metabolism by regulating downregulation, reducing reactive oxygen species production, and improving the natural cellular antioxidant defense system.

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Autophagy Behavior in Post-myocardial Infarction Injury.

Cardiovasc Hematol Disord Drug Targets

September 2023

Myocardial infarction and its sequalae remain the leading cause of death worldwide. Myocardial infarction (MI) survivors continue to live a poor quality of life due to extinguished heart failure. The post-MI period involves several changes at the cellular and subcellular levels, of which autophagy dysfunction.

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Undeniably, endothelial cells (EC) contribute to the maintenance of the homeostasis of the organism through modulating cellular physiology, including signaling pathways, through the release of highly active molecules as well as the response to a myriad of extrinsic and intrinsic signaling factors. Review the data from the current literature on the EC role in norm and disease. Endothelium maintains a precise balance between the released molecules, where EC dysfunction arises when the endothelium actions shift toward vasoconstriction, the proinflammatory, prothrombic properties after the alteration of nitric oxide (NO) production and oxidative stress.

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Neuron homeostasis is crucial for the organism, and its maintenance is multifactorial, including autophagy. The turnover of aberrant intracellular components is a fundamental pathogenetic mechanism for cell aging. Autophagy is involved in the acceleration of the neurocyte aging process and the modification of cell longevity.

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Endothelial cells (EC) are the anatomical boundaries between the intravascular and extravascular space. Damage to ECs is catastrophic and induces endothelial cell dysfunction. The pathogenesis is multifactorial and involves dysregulation in the signaling pathways, membrane lipids ratio disturbance, cell-cell adhesion disturbance, unfolded protein response, lysosomal and mitochondrial stress, autophagy dysregulation, and oxidative stress.

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Current advances in molecular pathobiology of endotheliocytes dysfunctions are promising in finding the pathogenetic links to the emergence of insulin resistance syndrome. Physiologically, human organism homeostasis is strictly controlled to maintain metabolic processes at the acquainted level. Many factors are involved in maintaining these physiological processes in the organism and any deviation is undoubtedly accompanied by specific pathologies related to the affected process.

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Basal autophagy plays a crucial role in maintaining intracellular homeostasis and prevents the cell from escaping the cell cycle regulation mechanisms and being cancerous. Mitophagy and nucleophagy are essential for cell health. Autophagy plays a pivotal role in cancer cell transformation, where upregulated precancerous autophagy induces apoptosis.

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Background And Aims: Metabolic syndrome is a multifactorial pathophysiological process with complicated homeostatic disorders that arise from various systematic metabolic defects. Various theories underlie the development of metabolic syndrome but are fully not understood.

Methods: Revising PubMed and Scopus literature data on metabolic syndrome pathogenesis and management.

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The post-COVID neurological syndrome has been coined, which describes the functional and structural sequelae of coronavirus infection disease-19 (COVID-19) in the brain. Mild/severe manifestations of the post-COVID neurological syndrome have been identified in approximately 33.00% of COVID-19 survivors.

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Myocardial cell injury and following sequelae are the primary reasons for death globally. Unfortunately, myocardiocytes in adults have limited regeneration capacity. Therefore, the generation of neo myocardiocytes from non-myocardial cells is a surrogate strategy.

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Recently, remarkable advances have been achieved in the molecular biopathology field and researchers turned to evaluate the role, molecular mechanisms, and clinical value of transcription factors in curing a variety of parenchymal degenerative pathologies. Special agents have the capability to cell lineage reprogramming termed transcription factors with a capacity for gene expression modification. Therefore, whatever niche factor may modify gene expression is termed as a transcription factor.

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