Aspirin Reduces Cardiac Interstitial Fibrosis by Inhibiting Erk1/2-Serpine2 and P-Akt Signalling Pathways

on MIce, but it would be good if it would replicate to humans.

Abstract
Background/aims: Cardiac interstitial fibrosis is an abnormality of various cardiovascular diseases, including myocardial infarction, hypertrophy, and atrial fibrillation, and it can ultimately lead to heart failure. However, there is a lack of practical therapeutic approaches to treat fibrosis and reverse the damage to the heart. The purpose of this study was to investigate the effect of long-term aspirin administration on pressure overload-induced cardiac fibrosis in mice and reveal the underlying mechanisms of aspirin treatment.

Methods: C57BL/6 mice were subjected to transverse aortic constriction (TAC), and treated with 10 mg·kg-1·day-1 of aspirin for 4 weeks. Masson staining and a collagen content assay were used to detect the effects of aspirin on cardiac fibrosis in vivo and in vitro. Western blot and qRT-PCR were applied to examine the impact of aspirin on extracellular signal-regulated kinases (Erks), p-Akt/β-catenin, SerpinE2, collagen I, and collagen III levels in the mice heart.

Results: Aspirin significantly suppressed the expression of α-smooth muscle actin (α-SMA; 1.19±0.19-fold) and collagen I (0.95±0.09-fold) in TAC mice. Aspirin, at doses of 100 and 1000 µM, also significantly suppressed angiotensin II-induced α-SMA and collagen I in cultured CFs. The enhanced phosphorylation of Erk1/2 caused by TAC (p-Erk1, 1.49±0.19-fold; p-Erk2, 1.96±0.68-fold) was suppressed by aspirin (p-Erk1, 1.04±0.15-fold; p-Erk2, 0.87±0.06-fold). SerpinE2 levels were suppressed via the Erk1/2 signalling pathway following treatment with aspirin (1.36±0.12-fold for TAC; 1.06±0.07-fold for aspirin+TAC). The p-Akt and β-catenin levels were also significantly inhibited in vivo and in vitro.

Conclusions: Our study reveals a novel mechanism by which aspirin alleviates pressure overload-induced cardiac interstitial fibrosis in TAC mice by suppressing the p-Erk1/2 and p-Akt/β-catenin signalling pathways


[pubmed.ncbi.nlm.nih.gov]

Good find Marco! Thanks
Aspirin is not usually GI friendly for a few and possibly poses a bleed factor if one is on a NOAC?? A family member has such a GI bleed from aspirin therapy that his affected bowels had to be removed.

There are reasons why I take 1/2 dose Eliquis instead of aspirin. Being only an animal study, I'll wait for confirming human studies to have an opinion on aspirin and fibrosis.

Human trials might ultimately alter those numbers one way or another, but some of them are quite modest with phosphorylation of Erk showing some promise.

Quote
susan.d
Good find Marco! Thanks
Aspirin is not usually GI friendly for a few and possibly poses a bleed factor if one is on a NOAC?? A family member has such a GI bleed from aspirin therapy that his affected bowels had to be removed.

Apirin is not usually GI friendly because it generally come with many bad fillers, but there is still out there some pure apirin

Aspirin itself can cause GI bleeds. It's not the fillers.