Following acute myocardial infarction (AMI), plasma progranulin levels exhibit a notable increase, which correlates with improved cardiac function, specifically an increase in left ventricular ejection fraction (LVEF) during the chronic phase. This finding, stemming from a prospective cohort study at Gifu Municipal Hospital, suggests a potential role for progranulin in cardiac recovery post-AMI.
The study, published in PLOS ONE, included 34 patients, 18 diagnosed with AMI and 16 controls. Blood samples were collected to measure plasma progranulin levels, and echocardiography was performed to assess LVEF, LV end-systolic dimension (LVSd), and LV end-diastolic dimension (LVDd). On day 0, progranulin levels were similar between the control group (69.5 ± 24.6 ng/mL) and the AMI group (84.2 ± 47.1 ng/mL). However, by day 7, progranulin levels in the AMI group significantly increased to 104.2 ± 52.0 ng/mL compared to the control group's 69.5 ± 24.6 ng/mL (p=0.045).
Progranulin's Role in Cardiac Repair
Progranulin, a secreted glycoprotein known for its role in regulating inflammation and wound healing, has previously demonstrated cardioprotective effects in animal models. Prior research indicated that progranulin administration reduced myocardial infarct size and improved left ventricular function in rabbits with AMI. This study extends these findings to humans, suggesting a similar mechanism may be at play.
"The increase in plasma progranulin levels during the acute phase of AMI was positively associated with the improvement in LVEF from the acute to the chronic phase," the researchers noted. This suggests that the body's natural response to myocardial infarction includes an increase in progranulin, potentially to aid in cardiac repair.
Limitations and Future Directions
The study acknowledges limitations, including a small sample size, which may affect the generalizability of the findings. Further research with larger cohorts is needed to validate these results and explore the underlying mechanisms by which progranulin influences cardiac function post-AMI. Understanding these mechanisms could pave the way for novel therapeutic strategies aimed at enhancing cardiac repair and improving outcomes for patients following myocardial infarction.
