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

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

6.0K
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...
6.0K
Feedback Inhibition00:46

Feedback Inhibition

57.2K
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!
57.2K
Complement System01:27

Complement System

10.8K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
10.8K
Complementation Tests00:49

Complementation Tests

6.3K
A complementation test is a simple cross to identify whether the two mutations are located on the same gene or different genes. It was first performed by Edward Lewis in the 1940s while working on fruit flies. He developed the test to identify the location and arrangement of different mutations on chromosomes.
Organisms heterozygous for different mutations are crossed pairwise in all combinations. If present on different genes, the mutations can complement each other by providing the missing...
6.3K
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

1.5K
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.5K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

1.2K
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
1.2K

You might also read

Related Articles

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

Sort by
Same author

Shiga toxin delivery in extracellular vesicles induces high mortality and severe kidney injury in a Gb3-dependent manner.

PLoS pathogens·2026
Same author

MicroRNAs as potential architects of immune dysregulation and megakaryocytic failure in immune thrombocytopenia.

British journal of haematology·2026
Same author

Cellular signaling pathway of Shiga toxin-induced ATP release.

Frontiers in cellular and infection microbiology·2026
Same author

Observational and Genetic Association of Myelodysplastic Syndromes (MDS) and Autoimmune Diseases in Adults.

Mediators of inflammation·2026
Same author

Association between anemia and stroke with its subtypes in adults: Insights from NHANES 2005-2016 and Mendelian randomization analyses.

Experimental gerontology·2025
Same author

Mitochondrial DNA via recipient TLR9 acts as a potent first hit in murine transfusion-related acute lung injury.

Blood·2025

Related Experiment Video

Updated: Feb 9, 2026

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

31.2K

Aliskiren inhibits renin-mediated complement activation.

Zivile D Békássy1, Ann-Charlotte Kristoffersson1, Johan Rebetz1

  • 1Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, Sweden.

Kidney International
|June 10, 2018
PubMed
Summary

Renin, a kidney enzyme, triggers complement activation by cleaving C3. The renin inhibitor aliskiren blocks this process, offering a potential therapeutic target for kidney diseases.

Keywords:
aliskirenchildrencomplementdense deposit diseasekidneyrenin

More Related Videos

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation
08:47

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

9.5K
Measuring the 50% Haemolytic Complement CH50 Activity of Serum
08:26

Measuring the 50% Haemolytic Complement CH50 Activity of Serum

Published on: March 29, 2010

38.9K

Related Experiment Videos

Last Updated: Feb 9, 2026

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

31.2K
Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation
08:47

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

9.5K
Measuring the 50% Haemolytic Complement CH50 Activity of Serum
08:26

Measuring the 50% Haemolytic Complement CH50 Activity of Serum

Published on: March 29, 2010

38.9K

Area of Science:

  • Nephrology
  • Immunology
  • Biochemistry

Background:

  • Kidney diseases are linked to complement activation, but the specific renal trigger remains unknown.
  • Complement system activation involves complex cascades with significant implications for renal health.

Purpose of the Study:

  • To identify the renal triggering factor for complement activation in certain kidney diseases.
  • To investigate the role of renin in initiating complement cascade.
  • To evaluate the efficacy of renin inhibition using aliskiren in mitigating complement activation.

Main Methods:

  • Demonstrated renin's ability to cleave complement component C3 into C3b and C3a, mimicking C3 convertase activity.
  • Utilized immunoblotting, N-terminal sequencing, and ELISA to detect and quantify C3 cleavage products.
  • Performed functional assays to assess C3a and C3b activity, including mast cell chemotaxis and factor Ba generation.
  • Investigated the effect of renin inhibition by aliskiren on C3 cleavage and C3 deposition in vitro and in patients.

Main Results:

  • Renin directly cleaves C3 into C3a and C3b, a process inhibited by aliskiren.
  • Renin-mediated C3 cleavage products initiate downstream complement activation pathways.
  • Aliskiren treatment in patients with dense deposit disease significantly reduced systemic and renal complement activation markers and renal pathology.

Conclusions:

  • Renin acts as a novel renal trigger for complement activation.
  • Aliskiren effectively inhibits renin-mediated complement activation, demonstrating therapeutic potential for kidney diseases.
  • Elevated intrarenal renin levels may explain the kidney's susceptibility to complement-mediated damage.