Exploration on the Effects of the IL- 6/Jak2/Stat3 Signaling Pathway on Myocardial Fibrosis and Heart Failure

Abstract

The IL-6/Jak2/Stat3 signaling pathway plays a crucial role in the pathogenesis and progression of myocardial fibrosis and heart failure. Its aberrant activation exacerbates inflammatory responses, cellular apoptosis, and fibrotic processes, ultimately impairing cardiac function. As a pro-inflammatory cytokine, IL-6 regulates cardiomyocyte survival, energy metabolism, and extracellular matrix remodeling via the Jak2/Stat3 pathway. In recent years, this signaling pathway has garnered significant research interest. Early studies have indicated that elevated IL-6 levels and excessive Stat3 activation are common in heart failure patients, while inhibition of Jak2 or Stat3 can attenuate fibrosis and improve cardiac function. Currently, targeted therapeutic strategies focusing on this pathway remain in an exploratory phase, with some interventions advancing to clinical trials. Future research should emphasize the cross-regulatory mechanisms of this signaling cascade and integrate artificial intelligence and big data analytics to develop personalized treatment strategies that enhance therapeutic efficacy while minimizing adverse effects. As investigations progress, targeted therapies directed at this pathway are expected to become a pivotal approach in the management of myocardial fibrosis and heart failure.