CARD9 Regulation and its Role in Cardiovascular Diseases
Haina Zhang1,2, Yeling Wang1, Hongbo Men1,2
1Department of Cardiovascular Diseases, First Hospital of Jilin University, Jilin University, Changchun, 130021, China.
Insights
Caspase recruitment domain-containing protein 9 (CARD9) is crucial for innate immunity and fungal defense. Its role in cardiovascular diseases (CVDs) involves inflammation, apoptosis, and autophagy, suggesting potential therapeutic targets.
Area of Science:
- Immunology
- Cardiovascular Biology
Background:
- Caspase recruitment domain-containing protein 9 (CARD9) is an adaptor protein in innate immunity, downstream of pattern recognition receptors (PRRs).
- CARD9 deficiency increases susceptibility to fungal infections.
- Emerging evidence links CARD9 to cardiovascular diseases (CVDs).
Purpose of the Study:
- To summarize CARD9's structure and function in innate immunity.
- To elucidate CARD9's roles in inflammation, apoptosis, and autophagy in CVD pathogenesis.
- To discuss potential CARD9-targeting therapies for CVDs.
Main Methods:
- Review of existing literature on CARD9 in innate immunity and CVDs.
- Analysis of CARD9's signaling pathways (p38 MAPK, NF-κB, NLRP3 inflammasome).
- Examination of CARD9's involvement in anti-apoptosis and autophagy in CVD models.
Main Results:
- CARD9 mediates pro-inflammatory cytokine and chemokine production in CVDs.
- CARD9 activation contributes to cardiac remodeling and dysfunction.
- CARD9 influences anti-apoptosis and autophagy, impacting CVD progression.
Conclusions:
- CARD9 plays a significant role in the pathogenesis of cardiovascular diseases.
- Targeting CARD9 pathways offers potential therapeutic strategies for CVD prevention.
- Further research is needed to fully understand CARD9's complex role in CVDs.
Abstract:
Caspase recruitment domain-containing protein 9 (CARD9) is an adaptor protein expressed on myeloid cells and located downstream of pattern recognition receptors (PRRs), which transduces signals involved in innate immunity. CARD9 deficiency is associated with increased susceptibility to various fungal diseases. Increasing evidence shows that CARD9 mediates the activation of p38 MAPK, NF-κB, and NLRP3 inflammasome in various CVDs and then promotes the production of proinflammatory cytokines and chemokines, which contribute to cardiac remodeling and cardiac dysfunction in certain cardiovascular diseases (CVDs). Moreover, CARD9-mediated anti-apoptosis and autophagy are implicated in the progression of CVDs. Here, we summarize the structure and function of CARD9 in innate immunity and its various roles in inflammation, apoptosis, and autophagy in the pathogenesis of CVDs. Furthermore, we discuss the potential therapies targeting CARD9 to prevent CVDs and raise some issues for further exploring the role of CARD9 in CVDs.
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