International Journal of Molecular Medical Science, 2025, Vol.15, No.1, 20-32 http://medscipublisher.com/index.php/ijmms 26 insufficiency, aiding in the digestion and absorption of nutrients (Bailey et al., 2020). Studies have shown that CFTR modulators can also positively impact nutritional status, with significant weight gain observed in patients treated with ivacaftor and ETI (Wu et al., 2018; Bailey et al., 2020). Patients with CF often require supplementation of vitamins and micronutrients, particularly fat-soluble vitamins (A, D, E, and K) due to malabsorption (Bailey et al., 2020). Antioxidant supplementation is also beneficial, as oxidative stress is a significant factor in the pathophysiology of CF. Vitamins C and E, in particular, have been shown to reduce oxidative damage and improve overall health outcomes in CF patients (Bailey et al., 2020; Zhou, 2024). 5.3 Anti-inflammatory treatments Chronic inflammation is a hallmark of CF, contributing to lung damage and disease progression. Current anti-inflammatory treatments include corticosteroids and Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) like ibuprofen, which have been shown to reduce inflammation and slow lung function decline (Hanrahan et al., 2019). However, long-term use of these drugs can lead to significant side effects, necessitating careful management (Hanrahan et al., 2019). Novel immunomodulatory agents are being explored to provide more targeted and effective anti-inflammatory effects with fewer side effects. These include drugs that modulate specific inflammatory pathways, such as those targeting interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α) (Hanrahan et al., 2019). Early studies suggest that these agents could offer significant benefits in reducing the metabolic burden and improving clinical outcomes in CF patients (Hanrahan et al., 2019). 6 Emerging Therapeutic Strategies Targeting Metabolic Pathways 6.1 Oxidative stress reduction Oxidative stress is a significant contributor to the pathophysiology of Cystic Fibrosis (CF), exacerbating lung damage and inflammation. Antioxidants such as N-acetylcysteine and Vitamin E have been explored to counteract this oxidative stress. N-acetylcysteine serves as a precursor to glutathione, a critical antioxidant that is often deficient in CF patients due to impaired CFTR function (Ntimbane et al., 2009; Moliteo et al., 2022). Vitamin E, a fat-soluble antioxidant, is also frequently deficient in CF patients due to malabsorption issues, and its supplementation has shown potential in reducing oxidative damage (Cantin et al., 2007; Causer et al., 2020). Studies have demonstrated that these antioxidants can help restore the balance between pro- and anti-oxidants, thereby mitigating oxidative stress and its associated cellular damage (Galli et al., 2012; Hewson et al., 2020). 6.2 Metabolic modulators CF patients often exhibit abnormalities in lipid metabolism, including imbalances in fatty acids. Lipid-based interventions aim to correct these imbalances and improve overall metabolic health. For instance, supplementation with essential fatty acids such as omega-3 and omega-6 has been shown to modulate inflammatory responses and improve lung function in CF patients (Causer et al., 2020; Moliteo et al., 2022). These interventions target the underlying metabolic disruptions caused by CFTR dysfunction, thereby offering a potential therapeutic strategy to alleviate some of the systemic complications of CF (Cantin et al., 2007; Hector et al., 2014). Cystic Fibrosis-Related Diabetes (CFRD) is a common and severe complication of CF, characterized by impaired glucose metabolism. Therapeutic agents targeting glucose metabolism, such as insulin and oral hypoglycemic agents, are crucial in managing CFRD. These agents help regulate blood glucose levels and mitigate the adverse effects of hyperglycemia on lung function and overall health (Ntimbane et al., 2009; Causer et al., 2020). Additionally, emerging therapies are exploring the use of incretin-based treatments and other metabolic modulators to improve insulin secretion and sensitivity in CF patients (Cantin et al., 2007; Galli et al., 2012). 6.3 Gene editing and RNA therapies Gene editing technologies, such as CRISPR/Cas9, have shown promise in correcting CFTR mutations at the genetic level. These technologies aim to repair the defective CFTR gene, thereby restoring its normal function. Preclinical studies have demonstrated the potential of CRISPR/Cas9 to correct specific CFTR mutations in cell
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