Scholarlink

<p>As an important transcription factor, activin receptor-like kinase 5 (ALK5) plays a crucial role in the development of various diseases. However, there have been no reports on whether ALK5 is involved in the pathogenesis of asthma, and further exploration is needed. An in vitro asthma model was constructed using house dust mite (HDM). Quantitative real-time polymerase chain reaction and western blot were used to detect the expression of ALK5. Enzyme-linked immunosorbent assays were used to measure the levels of inflammatory factors. Oxidative stress-related factors and glycolysis-related indicators were analysed using commercial kits. Co-immunoprecipitation was used to assess the binding activity of ALK5 and Krüppel-like factor 4 (KLF4). Finaly, an HDM-induced asthmatic mouse model was established. H&amp;E and PAS staining were used to evaluate the pathological status of mouse lungs, immunohistochemistry (IHC) was used to detect the expression of ALK5 and KLF4 in mouse lung tissue, and Masson staining was used to detect collagen deposition. The results showed that ALK5 was up-regulated in HDM-induced BEAS-2B cells. Silencing ALK5 suppressed inflammation and apoptosis in BEAS-2B cells. Furthermore, knockdown of ALK5 inhibited oxidative stress and promoted glycolysis in BEAS-2B cells. ALK5 specifically bound to KLF4 and promoted its protein degradation. Mechanistically, KLF4-mediated glycolysis was involved in the regulation of ALK5 in BEAS-2B cells. In vivo, ALK5 knockdown attenuated airway inflammation, reduced inflammatory cell infiltration, decreased collagen deposition, and improved lung histopathological damage. In conclusion, inhibiting ALK5 suppresses inflammation, apoptosis, and oxidative stress by regulating KLF4-mediated glycolysis in BEAS-2B cells, thus inhibiting the further development of asthma. Therefore, ALK5 may be a potential target for the clinical treatment of asthma.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

ALK5 inhibition reduces HDM-induced inflammation and oxidative injury by regulating KLF4-mediated glycolysis in BEAS-2B cells

  • 期刊论文

  • 发表日期：

    2026年2月15日

查看全文
  • Haixia Wang,
  • Kun Luo,
  • Shasha Li,
  • Dan Jin,
  • Ling Ou,
  • Cuicui Liu,
  • Qing Wu

摘要

As an important transcription factor, activin receptor-like kinase 5 (ALK5) plays a crucial role in the development of various diseases. However, there have been no reports on whether ALK5 is involved in the pathogenesis of asthma, and further exploration is needed. An in vitro asthma model was constructed using house dust mite (HDM). Quantitative real-time polymerase chain reaction and western blot were used to detect the expression of ALK5. Enzyme-linked immunosorbent assays were used to measure the levels of inflammatory factors. Oxidative stress-related factors and glycolysis-related indicators were analysed using commercial kits. Co-immunoprecipitation was used to assess the binding activity of ALK5 and Krüppel-like factor 4 (KLF4). Finaly, an HDM-induced asthmatic mouse model was established. H&E and PAS staining were used to evaluate the pathological status of mouse lungs, immunohistochemistry (IHC) was used to detect the expression of ALK5 and KLF4 in mouse lung tissue, and Masson staining was used to detect collagen deposition. The results showed that ALK5 was up-regulated in HDM-induced BEAS-2B cells. Silencing ALK5 suppressed inflammation and apoptosis in BEAS-2B cells. Furthermore, knockdown of ALK5 inhibited oxidative stress and promoted glycolysis in BEAS-2B cells. ALK5 specifically bound to KLF4 and promoted its protein degradation. Mechanistically, KLF4-mediated glycolysis was involved in the regulation of ALK5 in BEAS-2B cells. In vivo, ALK5 knockdown attenuated airway inflammation, reduced inflammatory cell infiltration, decreased collagen deposition, and improved lung histopathological damage. In conclusion, inhibiting ALK5 suppresses inflammation, apoptosis, and oxidative stress by regulating KLF4-mediated glycolysis in BEAS-2B cells, thus inhibiting the further development of asthma. Therefore, ALK5 may be a potential target for the clinical treatment of asthma.