2.5 The regulation of angiogenesis
In recent years, there is increasing evidence that pulmonary vascular
injury has become a major manifestation of BPD. Jing et al.found that
early caffeine treatment increased cAMP levels in a hyperoxicmodel of
lung injury, improved endothelial nitric oxide synthase (eNOS) activity
by inhibiting the degradation of GTP-cyclohydrolase-1, improved the
bioavailability of tetrahydrobiopterin(BH4), and improved alveolar
structure and vascular function72. In addition, Dumpa
et al.used male miceto show that caffeine can improve pulmonary vascular
remodeling in response to hyperoxia by increasing the vascular surface
area of small pulmonary arteries and by inhibiting smooth muscle
proliferation73. However, additional studies have
found that caffeine inhibits embryonic angiogenesis74;
therefore, furtherstudies are required to support the protective effects
of caffeine against pulmonary vascular injury.
In summary, the clinical benefits of caffeine have been confirmed,
although the molecular mechanisms responsible for its action remain
controversial and are still being investigated.Currently, research is
limited to five aspects: anti-inflammatory, antioxidant, anti-apoptotic,
and anti-fibrotic effects, and the regulation of angiogenesis. Caffeine
can act as a neurostimulant, thus leading to severe restrictions in the
clinical research process in many countries. In recent years, caffeine
has been shown to be protective against both Parkinson’s
disease75and colorectal cancer76by
regulating flora and autophagy; however, there is still significant
scope for investigating the effect of caffeine on BPD. This condition
affects the long-term survival of newborns; consequently, we need to
consider this disease carefully and find effective solutions for
prevention and treatment in order to promote human development.