The abstract is read at the publisher; the summary is JClub's.
CCR2-dependent monocyte recruitment is linked to progression from post-MI heart failure to pulmonary hypertension in mice, with RS102895 reducing lung vascular remodeling by 6 weeks.
- Why it matters: Myeloid inflammation is central in both post-MI responses and pulmonary hypertension, but whether systemic monocyte recruitment drives PH-LHD progression is unclear.
- What they did: The study measured inflammatory adhesion molecules (including VCAM1 and SELE) in human and rat PH-LHD, then induced MI and HF in C57BL/6J mice and treated HF mice with the CCR2 antagonist RS102895 from day 10 to assess PH-LHD at 6 weeks.
- The result: RS102895 attenuated lung vascular remodeling, right ventricular systolic and diastolic pressures, right ventricular hypertrophy, and lung adhesion molecule expression at 6 weeks versus vehicle, without improving left-sided HF.
The findingWhy it mattersWhat they didThe result
AI summary of the abstract · may contain errors · not medical advice · read the paper.