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Area of Science:

  • Cardiovascular Research
  • Inflammation and Immunology
  • Molecular Cardiology

Background:

  • Systemic inflammation is implicated in heart failure with preserved ejection fraction (HFpEF) pathogenesis, but its molecular mechanisms, particularly concerning systolic function, remain unclear.
  • While left ventricular (LV) diastolic dysfunction is primary in HFpEF, subclinical systolic dysfunction also contributes.
  • Previous studies linked collagen-induced arthritis (CIA) in rats to systemic inflammation, LV diastolic dysfunction, and elevated tumor necrosis factor-alpha (TNF-α), but not TNF-α mediation of diastolic dysfunction.

Purpose of the Study:

  • To investigate the impact of systemic inflammation and TNF-α blockade on systolic function in the CIA rat model.
  • To examine the effects on mRNA expression of genes involved in active LV diastolic relaxation and myosin heavy chain (MyHC) isoforms.

Main Methods:

  • Utilized the collagen-induced arthritis (CIA) rat model to induce systemic inflammation.
  • Administered TNF-α blockade to assess its protective effects.
  • Analyzed LV mRNA expression of genes related to diastolic function and MyHC isoforms (α-MyHC and β-MyHC).
  • Assessed LV global longitudinal strain and velocity to evaluate systolic function.

Main Results:

  • Collagen inoculation impaired LV global longitudinal strain and velocity (P < 0.05), indicating systolic dysfunction.
  • TNF-α blockade prevented the impairment of systolic function.
  • Collagen-induced inflammation decreased α-MyHC (Myh6) and increased β-MyHC (Myh7) mRNA expression (P < 0.05).
  • TNF-α blockade prevented this MyHC isoform shift.
  • No significant effects on mRNA expression of genes mediating active LV diastolic function were observed.

Conclusions:

  • Systemic inflammation, mediated by TNF-α, initiates early-stage left ventricular systolic dysfunction, not diastolic dysfunction, in the CIA rat model.
  • Increased circulating TNF-α alters MyHC isoform expression, favoring β-MyHC, which may underlie impaired contractile function and systolic dysfunction.
  • Targeting TNF-α may offer a therapeutic strategy for preventing inflammation-induced systolic dysfunction in HFpEF.