Related Experiment Video
Updated: Dec 13, 2025
07:37
An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
825
The ACE2-deficient mouse: A model for a cytokine storm-driven inflammation
Junyi Wang1,2, Nihal Kaplan2, Jan Wysocki3
1Department of Ophthalmology, The First Center of the PLA General Hospital, Beijing, China.
Summary
Mice lacking Angiotensin converting enzyme 2 (ACE2) developed age-related corneal cloudiness and inflammation. This ACE2 deficiency may offer a model for studying COVID-19 related eye conditions.
Area of Science:
- Ophthalmology
- Immunology
- Cardiovascular Research
Background:
- Angiotensin converting enzyme 2 (ACE2) regulates inflammation by converting angiotensin II (Ang II) to angiotensin 1-7 (Ang 1-7).
- ACE2's role in corneal tissue is largely unknown, despite its presence in many organs.
Purpose of the Study:
- To investigate the function of ACE2 in the cornea and its role in ocular inflammation.
- To explore the potential of ACE2-deficient mice as a model for COVID-19 related eye conditions.
Main Methods:
- Analysis of corneal phenotype in aging ACE2-deficient (Ace2-/-) mice.
- In vitro studies assessing cytokine and chemokine levels.
- Treatment experiments using an Angiotensin II type 1 receptor (AT1R) antagonist.
Main Results:
- Ace2-/- mice exhibited age-dependent corneal haze, edema, and neovascularization.
- Severe inflammation led to epithelial cell-fate changes and infiltration of immune cells into the stroma.
- Elevated inflammatory mediators (cytokines, chemokines) created a 'cytokine storm' phenotype, partially reversed by losartan.
Conclusions:
- ACE2 deficiency promotes corneal inflammation, potentially mediated by Ang II.
- The Ace2-/- mouse cornea serves as a valuable model for investigating COVID-19 ocular manifestations and potential treatments.
