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Cited by 90Nitric Oxide and Endothelin EffectsDiabetes, Cardiovascular Risks, and LipoproteinsDiet, Metabolism, and Disease

The DOI matches its Crossref record; 261 of the 262 references it cites were found in a registry or an index.

Endothelial dysfunction, platelet hyperactivity, hypertension, and the metabolic syndrome: molecular insights and combating strategies

Open access
Das, Diptimayee, Shruthi, Nagainallur Ravichandran, Banerjee, Antara, Jothimani, Ganesan, Duttaroy, Asim K., Pathak, Surajit·2023·Frontiers in Nutrition
DOI 10.3389/fnut.2023.1221438PMC PMC10442661
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Abstract

Metabolic syndrome (MetS) is a multifaceted condition that increases the possibility of developing atherosclerotic cardiovascular disease. MetS includes obesity, hypertension, dyslipidemia, hyperglycemia, endothelial dysfunction, and platelet hyperactivity. There is a concerning rise in the occurrence and frequency of MetS globally. The rising incidence and severity of MetS need a proactive, multipronged strategy for identifying and treating those affected. For many MetS patients, achieving recommended goals for healthy fat intake, blood pressure control, and blood glucose management may require a combination of medicine therapy, lifestyles, nutraceuticals, and others. However, it is essential to note that lifestyle modification should be the first-line therapy for MetS. In addition, MetS requires pharmacological, nutraceutical, or other interventions. This review aimed to bring together the etiology, molecular mechanisms, and dietary strategies to combat hypertension, endothelial dysfunction, and platelet dysfunction in individuals with MetS.

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Crossref · 10.3389/fnut.2023.1221438

Cites

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Figures

Figure 1 Insulin resistance due to oxidative stress is attributed to a disparity between the body’s antioxidant system and the generation of ROS, which in turn triggers inflammatory responses, atherosclerosis, hypertension, and myocardial infarction.
Figure 1 Insulin resistance due to oxidative stress is attributed to a disparity between the body’s antioxidant system and the generation of ROS, which in turn triggers inflammatory responses, atherosclerosis, hypertension, and myocardial infarction.CC BY · PubMed Central
Figure 2 Risk factors of MetS.
Figure 2 Risk factors of MetS.CC BY · PubMed Central
Figure 3 The mechanisms underlying endothelial dysfunction. The endothelial cells undergo oxidative stress due to alterations in their extracellular matrix layers caused by various factors such as aging, genetic predisposition, and environmental variables. The principal sources of ROS are NADPH oxidase and uncoupled nitric oxide synthase (NOS). The occurrence of endothelial function is attributed to an elevation in ROS beyond the innate antioxidant capabilities of the body. In addition, the production of substantial amounts of hydrogen peroxide (H2O2) contributes to the impairment of endothelial function and consequent cellular death.
Figure 3 The mechanisms underlying endothelial dysfunction. The endothelial cells undergo oxidative stress due to alterations in their extracellular matrix layers caused by various factors such as aging, genetic predisposition, and environmental variables. The principal sources of ROS are NADPH oxidase and uncoupled nitric oxide synthase (NOS). The occurrence of endothelial function is attributed to an elevation in ROS beyond the innate antioxidant capabilities of the body. In addition, the production of substantial amounts of hydrogen peroxide (H2O2) contributes to the impairment of endothelial function and consequent cellular death.CC BY · PubMed Central
Figure 4 Illustration of a series of processes involved in the hypertension mechanism.
Figure 4 Illustration of a series of processes involved in the hypertension mechanism.CC BY · PubMed Central
Figure 5 Thrombosis’s rapid spread due to circulating white blood cells and platelets. Endothelial cells release P-selectin through the exocytosis of Weibel Palade bodies (WPB) when stimulated by tumor necrosis factor alpha during inflammation. P-selectin glycoprotein ligand-1 (PSGL-1) recruits leukocytes such as neutrophils and monocytes by P-selectin. Neutrophil extracellular traps (NET) ensnare invaders, stimulate thrombus development, and activate platelets after being released by neutrophils. Platelets’ activation allows leukocytes to become activated and identify infections. Thrombus production is also encouraged by tissue factor (TF), which is released from the surface of monocytes and their microvesicles to initiate fibrin synthesis and red blood cell recruitment. The resultant thrombus aids in the entrapment of the infectious agent.
Figure 5 Thrombosis’s rapid spread due to circulating white blood cells and platelets. Endothelial cells release P-selectin through the exocytosis of Weibel Palade bodies (WPB) when stimulated by tumor necrosis factor alpha during inflammation. P-selectin glycoprotein ligand-1 (PSGL-1) recruits leukocytes such as neutrophils and monocytes by P-selectin. Neutrophil extracellular traps (NET) ensnare invaders, stimulate thrombus development, and activate platelets after being released by neutrophils. Platelets’ activation allows leukocytes to become activated and identify infections. Thrombus production is also encouraged by tissue factor (TF), which is released from the surface of monocytes and their microvesicles to initiate fibrin synthesis and red blood cell recruitment. The resultant thrombus aids in the entrapment of the infectious agent.CC BY · PubMed Central

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  1. Siracusa, Neuroinflammation and oxidative stress in the traumatic brain injury and in the pathogenesis of neurodegenerative diseases: modulation by nutritional Supplementation

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Metadata

Authors
Das, D., Shruthi, N. R., Banerjee, A., Jothimani, G., Duttaroy, A. K., & Pathak, S.
Affiliations
  • Chettinad Academy of Research and Education (IN)
  • University of Oslo (NO)
Corresponding author
  • Duttaroy, Asim K.
  • Pathak, Surajit
ORCID
Venue
Frontiers in Nutrition
Publisher
Frontiers Media SA
Published
2023-08-08
Volume
10
Pages
1221438-1221438
ISSN
2296-861X (ISSN-L)
DOI
10.3389/fnut.2023.1221438
PMC
PMC10442661
OpenAlex
W4385663817
Cited by
90
References
262
Citations by year
2026: 30 · 2025: 39 · 2024: 21
FWCI
3.21
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Nutrition (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • NORA - Norwegian Open Research Archives (submittedVersion, cc-by)
Funders
  • Universitetet i Oslo
  • Chettinad Academy of Research and Education
  • Medisinske fakultet, Universitetet i Oslo
Topics
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords
metabolic syndrome, endothelial dysfunction, platelet hyperreactivity, hypertension, obesity, dyslipidemia, hyperglycemia, atherosclerotic cardiovascular disease, molecular mechanisms, lifestyle modification, nutraceuticals, nutritional strategies, blood pressure control, glucose management

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