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

You might also read

Related Articles

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

Sort by
Same author

Deciphering Environmental Health Factors Behind Unknown Etiology of Chronic Kidney Disease in South Asia: Plans for Epidemiologic Study.

medRxiv : the preprint server for health sciences·2026
Same author

Bone morphogenetic proteins 4 and 7 increase human white and brown adipocyte thermogenic capacity.

JCI insight·2026
Same author

Phase 1 Study of Oral N-Acetylmannosamine in Primary Podocytopathies.

Kidney international reports·2026
Same author

Uric Acid Trajectories and CKD Progression in the African American Study of Kidney Disease and Hypertension.

Kidney international reports·2025
Same author

APOL1 Genotype and Patient Outcomes in US and South African Transplant Recipients With HIV who Received Kidneys From Donors With HIV.

Transplantation·2025
Same author

A Human Glomerular Disease Atlas defines the APOL1-JAK-STAT feed forward loop in focal segmental glomerulosclerosis.

medRxiv : the preprint server for health sciences·2025

Related Experiment Video

Updated: Oct 13, 2025

Use of a Piglet Model for the Study of Anesthetic-induced Developmental Neurotoxicity AIDN: A Translational Neuroscience Approach
06:38

Use of a Piglet Model for the Study of Anesthetic-induced Developmental Neurotoxicity AIDN: A Translational Neuroscience Approach

Published on: June 11, 2017

11.4K

Lessons From APOL1 Animal Models.

Teruhiko Yoshida1, Khun Zaw Latt1, Jurgen Heymann1

  • 1Kidney Disease Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (NIH), Bethesda, MD, United States.

Frontiers in Medicine
|November 12, 2021
PubMed
Summary
This summary is machine-generated.

African-Americans face higher chronic kidney disease risk due to APOL1 gene variants. This review examines APOL1 transgenic models to understand how these variants damage kidney cells.

Keywords:
APOL1CKD—chronic kidney diseaseanimal modelglomerular diseasespodocyte

More Related Videos

Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test
08:06

Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test

Published on: January 15, 2010

31.9K
Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

43.2K

Related Experiment Videos

Last Updated: Oct 13, 2025

Use of a Piglet Model for the Study of Anesthetic-induced Developmental Neurotoxicity AIDN: A Translational Neuroscience Approach
06:38

Use of a Piglet Model for the Study of Anesthetic-induced Developmental Neurotoxicity AIDN: A Translational Neuroscience Approach

Published on: June 11, 2017

11.4K
Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test
08:06

Murine Model for Parkinson's Disease: from 6-OH Dopamine Lesion to Behavioral Test

Published on: January 15, 2010

31.9K
Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
08:01

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits

Published on: March 16, 2016

43.2K

Area of Science:

  • Nephrology
  • Genetics
  • Molecular Biology

Background:

  • African-Americans exhibit a threefold higher incidence of chronic kidney disease (CKD) than European-Americans.
  • Genetic variants in the APOL1 gene, encoding apolipoprotein L1, are strongly associated with this increased CKD risk and are found predominantly in individuals of sub-Saharan African ancestry.
  • Despite the discovery of APOL1 renal risk variants a decade ago, the precise mechanisms by which APOL1 risk alleles induce glomerular cell damage remain largely unelucidated.

Purpose of the Study:

  • To review and synthesize findings from existing APOL1 transgenic models.
  • To critically evaluate the strengths and limitations of current transgenic models in elucidating APOL1's role in kidney disease.
  • To identify future research directions for understanding APOL1-associated nephropathy.

Main Methods:

  • This narrative review systematically examines published studies utilizing transgenic models (including flies, fish, and mice) to investigate APOL1 function and pathogenicity.
  • The review analyzes the reported cellular and physiological consequences of APOL1 risk variants in these models.
  • Key findings from cell culture studies are contrasted with evidence from in vivo transgenic systems.

Main Results:

  • Various transgenic models have provided insights into potential APOL1-mediated cellular damage pathways, including podocyte injury and endoplasmic reticulum stress.
  • However, translating findings from cell culture to these complex transgenic systems has proven challenging, with limited consensus on the primary mechanisms.
  • Limitations include differences in genetic background, model system specificities, and the difficulty in replicating the full spectrum of human disease phenotypes.

Conclusions:

  • APOL1 transgenic models offer valuable tools for dissecting the molecular mechanisms underlying APOL1 nephropathy.
  • Further refinement of these models is crucial to bridge the gap between in vitro observations and in vivo relevance.
  • Future research should focus on developing more sophisticated transgenic approaches to accurately recapitulate human APOL1-associated kidney disease and guide therapeutic strategies.