The hallmark of a variety of fibrotic diseases such as liver fibrosis, lung fibrosis, skin fibrosis and atherosclerosis is extensive extracellular matrix remodeling (ECMr) of the disease affected tissue. Inflammation often leads to tissue disruption and destruction, upon which locally released battery of proteases such as matrix metalloproteinases and cysteine proteases degrade the surrounding matrix. The degradation products of ECM proteins, the co-called neoepitopes, are released into the systemic circulation. By recent development of Enzyme-Linked Immunosorbent Assays (ELISAs) detecting the pathological tissue turnover in atherosclerosis and liver fibrosis, we have introduced a novel class of biomarkers into the field of fibrotic diseases, which have been proved efficient in the early diagnosis. This work has resulted in identification of common mechanisms involving specific cell types, proteins and proteases as well as pathways shared among the fibrotic diseases. In this analysis we seek to answer following questions: a) Are there common disease mechanisms and cell types involved in both atherosclerosis and fibrosis? b) Can the lessons learned in developing fibrosis biomarkers be used for the development of atherosclerosis biomarkers? Our hypothesis is that by answering the above questions, we may be able to improve general understanding of the early-stage disease initiation and progression of fibrotic diseases, which in turn may aid in early diagnosis, prognosis and ultimately patient management.