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Inflammation

Inflammation

Feedback Inhibition

Feedback Inhibition

Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!

Enzyme Inhibition

Enzyme Inhibition

Inhibitors are molecules that reduce enzyme activity by binding to the enzyme. In a normally functioning cell, enzymes are regulated by a variety of inhibitors. Drugs and other toxins can also inhibit enzymes. Some inhibitors bind to the enzyme’s active site, while others inhibit enzymatic activity by binding to other sites on the protein structure.

Target Cell Response to Hormones

Target Cell Response to Hormones

Hormones intricately bind to receptors on the surface or within target cells, initiating a cascade of cellular responses.
Notably, the cellular response can be regulated by altering the number of receptors expressed in the cell. For example, prolonged exposure to elevated hormone levels results in a gradual decline or down-regulation in the number of receptors for that specific hormone on the cell surface. Conversely, in response to low hormone levels, cells may use up-regulation, producing an...

Inhibition of Cdk Activity

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

Targeted Cancer Therapies

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...

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Related Experiment Video

Updated: Feb 4, 2026

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

Isorhyncophylline Targets PP2AC to Modulate YAP to Inhibit Endothelial Cell Inflammation.

Lihua Wang¹, Yuecheng Liu², Haichao Li¹

¹College of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan, China.

Phytotherapy Research : PTR

|February 2, 2026

Summary

Isorhynchophylline (IRN) from Uncaria rhynchophylla reduces atherosclerotic plaque and inflammation by targeting PP2AC and regulating YAP activity. This natural compound shows promise for treating atherosclerosis and related cardiovascular diseases.

Keywords:

PP2A YAP atherosclerosis endothelial cell inflammation isorhynchophylline

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Last Updated: Feb 4, 2026

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Published on: January 10, 2025

Area of Science:

Cardiovascular Medicine
Pharmacology
Molecular Biology

Background:

Atherosclerosis (AS) is a primary cause of cardiovascular diseases, leading to serious complications.
Isorhynchophylline (IRN), an alkaloid from Uncaria rhynchophylla, has anti-inflammatory effects but its role in AS is unknown.

Purpose of the Study:

To investigate the therapeutic potential and molecular mechanisms of Isorhynchophylline (IRN) in atherosclerosis.
To evaluate IRN's effects on endothelial inflammation and atherosclerotic plaque progression.

Main Methods:

Scratch wound healing and Transwell migration assays assessed cellular capabilities.
RT-PCR and western blot analyzed inflammation gene expression.
Molecular docking and drug affinity responsive target stability evaluated IRN-PP2AC binding.

Main Results:

IRN treatment significantly ameliorated atherosclerotic plaque progression.
IRN mitigated endothelial inflammation.
IRN binds to PP2AC, subsequently regulating YAP activity.

Conclusions:

Isorhynchophylline (IRN) demonstrates therapeutic potential for atherosclerosis by reducing inflammation.
The mechanism involves IRN binding to PP2AC and modulating YAP activity.
IRN shows promise as a novel treatment for AS and associated cardiovascular conditions.