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 Experiment Videos

CRRL269.

Yang Chen1,2, Gail J Harty1, Ye Zheng1

  • 1From the Cardiorenal Research Laboratory, Department of Cardiovascular Medicine (Y.C., G.J.H., Y.Z., S.R.I., S.S., S.J.S., T.I., J.C.B.), Mayo Clinic, Rochester, MN.

Circulation Research
|April 2, 2019
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

C-Type Natriuretic Peptide and Cardiovascular-Renal Protection in Sepsis.

Hypertension (Dallas, Tex. : 1979)·2026
Same author

Functional evaluation of TRPC6 missense variants in cancer patients via molecular docking analysis compared with patch Clamp electrophysiology.

The Journal of biological chemistry·2026
Same author

Gain-of-Function Variant <i>TRPC6 A404V</i> Is Associated With Doxorubicin-Related Cardiomyopathy.

Circulation. Genomic and precision medicine·2026
Same author

Functional Evaluation of <i>TRPC6</i> Missense Variants in Cancer Patients via Molecular Docking Analysis Compared with Patch Clamp Electrophysiology.

bioRxiv : the preprint server for biology·2026
Same author

The Concise Guide to PHARMACOLOGY 2025/26: Catalytic receptors.

British journal of pharmacology·2025
Same author

Effects of physiological doses of atrial natriuretic peptide on lipolysis, ketogenesis, and glucose metabolism in men.

American journal of physiology. Endocrinology and metabolism·2025
Same journal

SBK2 Links Cardiac Stress Signaling to Mitochondrial Proteostasis.

Circulation research·2026
Same journal

Myeloid Piezo1 as a Brake on Efferocytosis and Cardiac Repair in the Infarcted Heart.

Circulation research·2026
Same journal

Targeting Late Na<sup>+</sup> Current: Too Late or Better Late Than Never?

Circulation research·2026
Same journal

HFpEF-Any: Human Single-Nuclear Transcriptomics Challenging the Translational Validity of Current HFpEF Models.

Circulation research·2026
Same journal

Myovascular Niche: The Role of Endothelial Cells in Skeletal Muscle Health and Disease.

Circulation research·2026
Same journal

Meet the First Authors.

Circulation research·2026
See all related articles
This summary is machine-generated.

A novel drug, CRRL269, shows promise for treating acute kidney injury (AKI) by protecting the heart and kidneys without causing hypotension. This study also identified urinary C-type natriuretic peptide (uCNP) as a potential biomarker for AKI.

Area of Science:

  • Nephrology
  • Cardiology
  • Pharmacology

Background:

  • Acute kidney injury (AKI) is prevalent in critically ill patients, increasing heart failure risk.
  • Existing treatments for AKI are limited, with no FDA-approved drugs.
  • Endogenous particulate guanylyl cyclase A (pGC-A) activators show potential but cause hypotension.

Purpose of the Study:

  • To investigate the therapeutic potential of CRRL269, a nonhypotensive pGC-A activator, in a canine model of ischemia-induced AKI.
  • To evaluate CRRL269's renocardiac protective effects and its impact on hemodynamic parameters.
  • To explore urinary C-type natriuretic peptide (uCNP) as a potential biomarker for AKI.

Main Methods:

  • Administered CRRL269 to a canine model of ischemia-induced AKI.
Keywords:
acute kidney injuryapoptosiscardiorenal syndromeheart failurenatriuretic peptide

Related Experiment Videos

  • Measured cGMP generation, plasma angiotensin II, cardiac filling pressures, and blood pressure.
  • Assessed glomerular filtration rate, renal blood flow, diuresis, natriuresis, kidney injury, and apoptosis.
  • Analyzed intracellular Ca2+ concentration and gene expression related to apoptosis.

    • Main Results:

    • CRRL269 increased cGMP, suppressed angiotensin II, and reduced cardiac filling pressures without lowering blood pressure.
    • CRRL269 preserved renal function, enhanced renal blood flow, and promoted diuresis and natriuresis.
    • CRRL269 reduced kidney injury and apoptosis, demonstrating potent antiapoptotic effects in renal cells.
    • AKI was associated with increased uCNP levels, suggesting its potential as a biomarker.

    Conclusions:

    • CRRL269 demonstrates significant renocardiac protective effects in an AKI model.
    • CRRL269's ability to avoid hypotension makes it a promising therapeutic candidate.
    • The study supports the development of CRRL269 as a novel treatment for AKI.
    • uCNP may serve as a valuable biomarker for detecting and monitoring AKI.