Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
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...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
Human Genetics01:28

Human Genetics

Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
The complex relationship between genetics and psychology is observable through common biological components such...
Pharmacogenomics: Identification of New Drug Targets01:29

Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Unraveling jasmonic acid-mediated mitigation of 6PPD toxicity in tomato plants using multi-omics approaches.

Journal of hazardous materials·2026
Same author

Bioremediation of textile effluents by <i>Serratia liquefaciens</i> AM-2 for subsequent use in crop production.

3 Biotech·2026
Same author

<i>In vitro</i> digestion-based study of heavy metal accumulation and bioaccessibility in organs of different chicken breeds.

Food & function·2026
Same author

Computational design and experimental validation of peptide inhibitors to disrupt urease enzyme maturation in pathogenic bacteria <i>Proteus mirabilis</i>.

Journal of biomolecular structure & dynamics·2026
Same author

Integrated Pharmacophore, Docking, Machine Learning, and Molecular Dynamics Approach for the Discovery and Validation of LuxS Quorum-Sensing Inhibitors to Combat Antibiotic Resistance.

ChemPlusChem·2026
Same author

Comparative efficacy of foliar-applied biogenic copper and iron nanoparticles for mitigating salinity stress in chickpea (<i>Cicer arietinum L.</i>).

International journal of phytoremediation·2026

Related Experiment Videos

Elevated interleukin-36γ and gene polymorphisms implicate novel risk in essential hypertension.

Alishba Kainat1, Fazlul Aziz Mian2, Muhammad Asif Nawaz Khan2

  • 1Department of Biosciences, COMSATS University Islamabad, Islamabad, 45550, Pakistan.

Immunogenetics
|July 5, 2026
PubMed
Summary

Elevated interleukin-36 gamma (IL-36γ) levels and IL36G gene variants are significantly associated with essential hypertension risk. Higher IL-36γ may contribute to hypertension development, showing potential as a clinical biomarker.

Keywords:
AssociationEssential HypertensionGenotypingIL-36Polymorphism

Related Experiment Videos

Area of Science:

  • Cardiovascular Research
  • Genetics and Genomics
  • Immunology

Background:

  • Cytokines, including IL-36γ, are implicated in hypertension and vascular inflammation.
  • The role of IL-36γ in essential hypertension remains largely unexplored despite its association with other cardiovascular diseases.

Purpose of the Study:

  • To investigate the clinical significance of serum IL-36γ levels and IL36G gene variants in relation to essential hypertension risk.
  • To explore the potential of IL-36γ as a diagnostic biomarker for essential hypertension.

Main Methods:

  • Serum IL-36γ levels were measured using enzyme-linked immunosorbent assay (ELISA).
  • IL36G gene polymorphisms (rs11690399 and rs11683399) were analyzed using PCR-RFLP in 264 essential hypertension patients and 264 controls.
  • Mendelian randomization and ROC analysis were employed to assess causality and diagnostic performance.

Main Results:

  • Patients with essential hypertension exhibited significantly higher serum IL-36γ levels compared to normotensive controls (p < 0.0001).
  • Specific IL36G polymorphisms (rs11690399 and rs11683399) were significantly associated with essential hypertension susceptibility.
  • A causal relationship was established between increased IL-36γ and hypertension risk (OR = 1.0066), with IL-36γ demonstrating good diagnostic performance (AUC = 0.862).

Conclusions:

  • Higher circulating IL-36γ levels and specific IL36G gene variants are significantly associated with essential hypertension.
  • Elevated IL-36γ may play a crucial role in the pathophysiology of essential hypertension.
  • IL-36γ shows promise as a potential clinical biomarker for essential hypertension diagnosis.