Hello! You are correct in evaluating types I and III collagens and TGF beta. In our laboratory, when studying cardiac remodeling, we also evaluated the expression of connexin 43, parameters of cellular hypertrophy, and cardiac electrophysiology.

Adverse post-MI LV remodeling can be evaluated at different levels:

- Anatomical level: LV dilatation (increase in LV end-diastolic volume and LV end-systolic volumes), LV hypertrophy (increase in LV mass), architectural / geometrical remodeling (the LV loses its usual elongated, gullet-like shape and acquires a more spherical configuration, you can use sphericity index for this)

- Neurohormonal level: Sympathetic system overdrive (increase in adrenaline/noradrenaline levels), enhancement of RAAS system (higher levels of angiotensin II or aldosterone), raise in BNP (neurohormone marking LV dilatation)

- Histological level in the remote non-infarcted tissue: Cardiomyocyte hypertrophy (using staining for vinculin or wheat hemagglutinin), interstitial fibrosis (staining for picrosirius red), capillary paucity (staining for CD31 or isolectin)

- Molecular level: Activation (phosphorylation) of Akt/ERK/p38 (which drive cardiomyocyte hypertrophy), molecular markers of fibrosis (collagen I/III, CTGF, TGF-beta)

- Metabolism/energetic levels: Healthy myocardium predominantly consumes free fatty acid to generate ATP. There is a shift, however, in cardiac metabolism in remodeled myocardium towards mainly using glucose instead of free fatty acids