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Crosslink breakers: a new approach to cardiovascular therapy
Dinko Susic1, Jasmina Varagic, Jwari Ahn
1Hypertension Research Laboratory, Ochsner Clinic Foundation, New Orleans, Louisiana 70121, USA. dsusic@ochsner.org
Current Opinion in Cardiology
|June 26, 2004
Summary
Advanced glycation end-products (AGEs) cause harmful protein crosslinks. A new drug, ALT-711, breaks these AGEs-related crosslinks, showing promise for treating cardiovascular and kidney issues in aging and diabetes.
Area of Science:
- Biochemistry
- Cardiovascular Science
- Nephrology
Background:
- Advanced glycation end-products (AGEs) accumulate with aging and high glucose.
- AGEs increase protein crosslinking, leading to cardiovascular stiffness and morbidity.
- Increased collagen crosslinking contributes to cardiovascular and renal dysfunction.
Purpose of the Study:
- To review evidence on breaking AGEs-related collagen crosslinks as a therapeutic strategy.
- To summarize the effects of ALT-711 on cardiovascular and renal health.
- To explore ALT-711's potential in managing aging and diabetes-related complications.
Main Methods:
- Review of recent experimental studies and one clinical trial.
- Analysis of data on ALT-711's impact on cardiovascular and renal parameters.
- Investigation of potential mechanisms of action, including oxidative stress and profibrotic cytokines.
Main Results:
- ALT-711 ameliorated cardiovascular and renal changes in aging, diabetic, and hypertensive models.
- In diabetic animals, ALT-711 improved cardiac function, reduced aortic stiffness, and enhanced renal function.
- In hypertensive rats, ALT-711 reduced cardiac mass, proteinuria, and extended survival.
Conclusions:
- Breaking AGEs-related collagen crosslinks with ALT-711 is a viable therapeutic approach.
- ALT-711 shows significant promise for treating cardiovascular and renal disorders.
- This strategy offers a new avenue for managing complications associated with aging, diabetes, and hypertension.