LCN2: A Potential Drug Target and Biomarker for the Treatment of Osteoarthritis

Target Name: LCN2

NCBI ID: G3934

LCN2

LCN2: A Potential Drug Target and Biomarker for the Treatment of Osteoarthritis

Osteoarthritis (OA) is a leading cause of pain and disability in adults, affecting millions of people worldwide. The condition is characterized by the wear and tear of joint tissue, leading to inflammation, pain, and reduced mobility. There are several treatment options available for OA, including non-steroidal anti-inflammatory drugs (NSAIDs), joint supplements, and biologic agents. However, these treatments have several drawbacks, including potential side effects and limited efficacy. As a result, there is a growing interest in identifying new drug targets and biomarkers for the treatment of OA.

LCN2: A Potential Drug Target and Biomarker

The 25 kDa alpha-2-microglobulin-related subunit of MMP-9 (LCN2) has been identified as a potential drug target and biomarker for the treatment of OA. MMP-9 is a protein that is expressed in high levels in the synovial fluid of OA patients, and it has been shown to play a role in the development and progression of the condition. The 25 kDa alpha-2-microglobulin-related subunit of MMP-9 (LCN2) is a small protein that is derived from the MMP-9 protein and is expressed in high levels in the synovial fluid of OA patients.

LCN2 has been shown to interact with several cellular signaling pathways that are involved in the development and progression of OA. For example, Lcn2 has been shown to interact with the TGF-β pathway, which is involved in the development of OA joint tissue inflammation and pain. Additionally, Lcn2 has been shown to interact with the NF-kappa-B pathway, which is involved in the production of pro-inflammatory cytokines that contribute to OA pain and inflammation.

LCN2 has also been shown to play a role in the production of pain signals in OA patients. In a study published in the Journal of Biological Chemistry, researchers found that Lcn2 was involved in the production of pain signals in OA joints. This suggests that Lcn2 may be a useful biomarker for the assessment of OA pain.

LCN2 has also been shown to be expressed in the synovial fluid of OA patients and has been used as a sample for diagnostic studies. In a study published in the Arthritis Care & Research, researchers found that Lcn2 was expressed in the synovial fluid of OA patients and was associated with the development of OA. This suggests that Lcn2 may be a useful sample for diagnostic studies of OA and could be used as a biomarker for the condition.

Conclusion

LCN2 has been identified as a potential drug target and biomarker for the treatment of OA. The evidence suggests that Lcn2 plays a role in the development and progression of OA and is involved in the production of pain signals in OA joints. Further research is needed to determine the effectiveness of Lcn2 as a drug target and biomarker for the treatment of OA. If Lcn2 is found to be effective, it may be a useful addition to the treatment options available for OA patients.

Protein Name: Lipocalin 2

Functions: Iron-trafficking protein involved in multiple processes such as apoptosis, innate immunity and renal development (PubMed:12453413, PubMed:27780864, PubMed:20581821). Binds iron through association with 2,3-dihydroxybenzoic acid (2,3-DHBA), a siderophore that shares structural similarities with bacterial enterobactin, and delivers or removes iron from the cell, depending on the context. Iron-bound form (holo-24p3) is internalized following binding to the SLC22A17 (24p3R) receptor, leading to release of iron and subsequent increase of intracellular iron concentration. In contrast, association of the iron-free form (apo-24p3) with the SLC22A17 (24p3R) receptor is followed by association with an intracellular siderophore, iron chelation and iron transfer to the extracellular medium, thereby reducing intracellular iron concentration. Involved in apoptosis due to interleukin-3 (IL3) deprivation: iron-loaded form increases intracellular iron concentration without promoting apoptosis, while iron-free form decreases intracellular iron levels, inducing expression of the proapoptotic protein BCL2L11/BIM, resulting in apoptosis (By similarity). Involved in innate immunity; limits bacterial proliferation by sequestering iron bound to microbial siderophores, such as enterobactin (PubMed:27780864). Can also bind siderophores from M.tuberculosis (PubMed:15642259, PubMed:21978368)

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