From the Research
High ACE levels and NLRP3 may have an indirect relationship through their involvement in inflammatory processes, though direct evidence linking them is limited, as suggested by the most recent study in 2025 1. The relationship between high Angiotensin-Converting Enzyme (ACE) levels and NLRP3 (Nucleotide-binding domain, leucine-rich repeat-containing protein 3) is complex and not fully understood. ACE plays a crucial role in the renin-angiotensin system, regulating blood pressure and fluid balance. Elevated ACE levels are associated with hypertension and cardiovascular issues, which often involve chronic inflammation. NLRP3, on the other hand, is a key component of the inflammasome, a protein complex that triggers inflammatory responses as part of the innate immune system.
Some key points to consider:
- NLRP3 inflammasome activation is involved in various inflammatory diseases, including cardiovascular diseases, as discussed in a 2020 review 2.
- The NLRP3 inflammasome has been implicated in the pathogenesis of atherosclerosis, ischemia/reperfusion injury, and heart failure, as noted in a 2020 study 2.
- A 2024 study discovered a potent brain-penetrant inhibitor of the NLRP3 inflammasome, NP3-253, which may have therapeutic potential for treating inflammatory diseases 3.
- The role of mitochondria in regulating NLRP3 inflammasome activity is still unclear, with some studies suggesting a central role for mitochondria in NLRP3 activation, as discussed in a 2014 review 4.
- NLRP3 inflammasome activation has been linked to inflammatory bowel diseases, with a 2017 study demonstrating the pathogenic role of NLRP3 inflammasome activation in inflammatory bowel diseases of both mice and humans 5.
- The most recent study in 2025 found that NLRP3 inflammasome-modulated angiogenic function of endothelial progenitor cells (EPC) via the PI3K/Akt/mTOR pathway in diabetic myocardial infarction, suggesting a potential therapeutic target for improving myocardial infarction repair in inflammatory diseases 1.
Overall, while there is no direct evidence linking high ACE levels and NLRP3, the shared involvement in inflammatory pathways suggests a potential indirect relationship. Further research is needed to confirm and characterize any specific relationship between high ACE levels and NLRP3 activity.