Related Experiment Video

Updated: May 7, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

13.0K

[Tumor necrosis factor alfa in cardiovascular diseases: molecular biology and genetics]

José Manuel Fragoso Lona1, Mónica Sierra Martínez, Gilberto Vargas Alarcón

  • 1Departamento de Biología Molecular, Instituto Nacional de Cardiología «Ignacio Chávez», México, D.F. dr.julian.ramirez.inv@gmail.com.

Gaceta Medica De Mexico
|October 11, 2013
PubMed

Insights

Tumor necrosis factor alpha (TNF-α) plays a key role in coronary artery disease (CAD) development and progression. Genetic variations in TNF-α influence CAD susceptibility, severity, and treatment outcomes.

Area of Science:

  • Immunology
  • Cardiology
  • Genetics

Context:

  • Cardiovascular diseases (CVDs) are a leading global health issue, causing significant mortality and morbidity.
  • In the US, CVDs accounted for 41% of deaths in 1997, affecting approximately 60 million individuals.
  • CVDs are chronic inflammatory conditions linked to immune system dysregulation.

Purpose:

  • To review the biological role of tumor necrosis factor alpha (TNF-α) in the initiation and progression of endothelial dysfunction.
  • To summarize evidence on how TNF-α contributes to atherosclerosis complications.
  • To examine the impact of TNF-α genetic variations on coronary artery disease (CAD) susceptibility, severity, and treatment response.

Summary:

  • Tumor necrosis factor alpha (TNF-α), a potent cytokine, is implicated in the inflammatory processes underlying CAD.
  • Evidence suggests TNF-α drives endothelial dysfunction and atherosclerotic complications.
  • Genetic variations in the TNF-α gene are associated with varying susceptibility, disease severity, and response to treatments in CAD patients, including myocardial infarction and angina.

Impact:

  • Highlights TNF-α as a critical factor in cardiovascular disease pathogenesis.
  • Underscores the potential of targeting TNF-α or its genetic variations for improved CAD management and treatment strategies.
  • Provides a foundation for further research into the genetic and inflammatory underpinnings of coronary artery disease.

More Related Videos

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

10.1K
Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo08:19

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

Published on: July 20, 2019

5.3K

Related Concept Videos

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
769
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.9K
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
84
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
1.1K
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
160
Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
911