Based on the provided search results, nuclear proteins, particularly **nuclear factor-κB (NF-κB)** and **protein kinase C (PKC)**, appear to play a significant role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Here’s a synthesis of the key findings:

### 1. **NF-κB Activation in COPD**

- A study comparing lung tissue from COPD patients and non-COPD controls found that **NF-κB p65** (a subunit of the NF-κB transcription factor) was significantly more active in COPD patients. Specifically:

- **Nuclear localization of NF-κB p65** was higher in COPD patients, indicating increased transcriptional activity .

- **NF-κB/DNA binding activity** was approximately **3.2 times higher** in COPD patients compared to controls .

- This activation correlated negatively with **arterial oxygen levels (PaO₂)**, suggesting a link between NF-κB and disease severity .

### 2. **Protein Kinase C (PKC) Involvement**

- The same study observed elevated levels of **PKCα** (a subtype of PKC) in COPD lung tissue:

- Both **PKCα mRNA and protein expression** were significantly higher in COPD patients .

- PKC is known to activate NF-κB, suggesting a potential **PKC-NF-κB signaling axis** in COPD progression .

### 3. **Implications for COPD Pathogenesis**

- NF-κB regulates genes involved in **inflammation, oxidative stress, and apoptosis**, all of which are key mechanisms in COPD .

- The upregulation of PKC and NF-κB may contribute to **chronic inflammation** and **tissue remodeling** seen in COPD patients .

### 4. **Nuclear Receptors and Lipid Metabolism (Indirect Relevance)**

- While not directly studied in COPD, the second article discusses **nuclear receptors** (e.g., PPARs, glucocorticoid receptors) as regulators of lipid metabolism and inflammation . Since COPD involves systemic inflammation and metabolic dysregulation, these receptors could theoretically influence disease progression, though direct evidence is lacking in the provided search results.

### **Conclusion**

The available evidence strongly suggests that **nuclear proteins like NF-κB and PKC are upregulated in COPD** and contribute to its inflammatory and destructive processes. Targeting these pathways (e.g., with PKC or NF-κB inhibitors) could be a potential therapeutic strategy, though further research is needed .

For more details, you may refer to the original study on PKC and NF-κB in COPD lung tissue .