Circulating Biomarkers of Cardiac Fibrosis: From Bench to Bedside

Heart disease remains one of the leading health challenges of the 21st century, with modern lifestyles only amplifying its global impact. Among its many contributors, cardiac fibrosis plays a crucial yet sometimes overlooked role (1). Detecting and managing fibrosis early can be considered essential for preventing fundamental cardiac damage (2). While imaging techniques have advanced, researchers are increasingly turning to the blood for answers. The identification of circulating biomarkers offers a promising avenue for improving diagnosis, guiding treatment, and monitoring disease progression.

When the myocardium experiences injury, such as that caused by myocardial infarction, the pro-fibrotic signalling pathways are activated (3). The resulting reparative response ultimately causes the deposition of excess collagen, replacing the lost cardiomyocytes with dense, fibrous tissue. Over time, the repeated activation of this cycle causes pathological remodelling of the extracellular matrix, hindering cardiac function and increasing likelihood of cardiovascular disease and heart failure (3). This cascade so far remains largely impervious to therapeutic interventions and can remain initially undetected due to limitations in the currently available diagnostic methods (1, 2, 4). Focusing research efforts on the identification of novel circulating biomarkers capable of characterizing and monitoring cases of cardiac fibrosis may therefore be critical for improving diagnosis and patient outcomes (5).

As a result, research has taken the path of looking into biomarkers which can provide an indication of the fibrotic activity in the heart. Several biomarkers have already been well established. Galectin-3 for example has been found to be a useful predictive marker of future cardiac events and directly correlates with the degree of myocardial fibrosis (6). In some cases, it has even been able to differentiate between subtypes of fibrotic heart disease, allowing for more personalized therapeutic interventions (2). B-type Natriuretic Peptide and N-Terminal Pro-B-Type Natriuretic Peptide, which are released in response to ventricular stretch and injury, are traditional markers of heart failure (7). Although they are not fibrosis specific, they can complement the use of other fibrosis biomarkers, helping clinicians assess responses to therapeutic interventions and determine disease severity.

Beyond these established markers, ongoing research continues to explore novel circulating biomarkers for cardiac fibrosis. The process of cardiac remodelling primarily involves myocardial fibrillar collagen types I (COL1) and III (COL3) (5). Abnormal accumulation of these collagens can lead to the release of collagen-derived peptides, such as the N-terminal propeptide of type III procollagen (PIIINP), into the circulation (8). As circulating PIIINP levels correlate with myocardial fibrosis, it has been investigated as a prognostic marker for heart failure and other fibrosis-related cardiac diseases (9). These findings suggest that measuring collagen-derived peptides may be used as a marker to monitor fibrotic activity and assess disease progression, highlighting just one promising avenue for future clinical applications.

Detecting cardiac fibrosis before irreversible damage occurs remains a major clinical challenge, largely due to the limitations posed by current imaging techniques and routine examinations. While several circulating biomarkers have already demonstrated value in assessing disease progression and risk, others are still emerging with considerable promise. With continued clinical research and well-designed trials, these biomarkers have the potential to bridge the gap between experimental findings and real-world clinical practice. Whether through a multi-omic approach, or the development of combined biomarker panels that capture the broader biological picture, advancing this field could have a fundamental impact on the way cardiac fibrosis is detected and managed. Ultimately, progress in circulating biomarker research represents one of the most promising avenues for reducing the growing global burden of cardiac disease.

 

At Abbexa, we have a large catalogue of tools for cardiovascular research, including ELISA kitsproteins, antibodies, and assays targeting biomarkers such as Galectin-3, BNP, NT-proBNP, COL1/COL3 peptides, PIIINP and more:

ELISA kits Antibodies  Proteins
Human Galectin 3 (LGALS3) ELISA Kit (abx250728) Galectin 3 (LGALS3) Antibody (abx132483) Human Galectin 3 (LGALS3) Protein (abx066731)
Human Brain Natriuretic Peptide (BNP) ELISA Kit (abx252095) Natriuretic Peptide Precursor B (NPPB) Antibody (abx132143) Mouse Natriuretic Peptide Precursor B (NPPB) Protein (abx652102)
Human N-Terminal Pro-C-Type Natriuretic Peptide (NT-ProCNP) ELISA Kit (abx152561) N-Terminal Pro-Brain Natriuretic Peptide (NT-ProBNP) Antibody (abx132145) Dog N-Terminal Pro-Brain Natriuretic Peptide (NT-ProBNP) Protein (abx652099)
Human Collagen Type III (COL3) ELISA Kit (abx151126) Collagen Type I Alpha 1 (COL1A1) Antibody (abx171831) Human Collagen Type I Alpha 1 (COL1A1) Protein (abx657212)
Chicken Procollagen Type III N-Terminal Propeptide (PIIINP) ELISA Kit (abx356255) Procollagen Type III N-Terminal Propeptide (PIIINP) Antibody (abx132509) Human Procollagen Type III N-Terminal Propeptide (PIIINP) Protein (abx168651)

 

 

If you’re looking for something specific, contact us for a custom solution for your research.

 

References: 

  1. BaniHani, H. A., Khaled, L. H., Al Sharaa, N. M., Al Saleh, R. A., Bin Ghalaita, A. K., Bin Sulaiman, A. S., & Holeihel, A. (2025). Causes, Diagnosis, Treatment, and Prognosis of Cardiac Fibrosis: A Systematic Review. Cureus, 17(3), e81264. https://doi.org/10.7759/cureus.81264
  2. Frangogiannis N. G. (2021). Cardiac fibrosis. Cardiovascular research, 117(6), 1450–1488. https://doi.org/10.1093/cvr/cvaa324
  3. Ghazal, R., Wang, M., Liu, D., Tschumperlin, D. J., & Pereira, N. L. (2025). Cardiac Fibrosis in the Multi-Omics Era: Implications for Heart Failure. Circulation research, 136(7), 773–802. https://doi.org/10.1161/CIRCRESAHA.124.325402
  4. Klappacher, G., Franzen, P., Haab, D., Mehrabi, M., Binder, M., Plesch, K., Pacher, R., Grimm, M., Pribill, I., & Eichler, H. G. (1995). Measuring extracellular matrix turnover in the serum of patients with idiopathic or ischemic dilated cardiomyopathy and impact on diagnosis and prognosis. The American journal of cardiology, 75(14), 913–918. https://doi.org/10.1016/s0002-9149(99)80686-9
  5. Liu, M., López de Juan Abad, B., & Cheng, K. (2021). Cardiac fibrosis: Myofibroblast-mediated pathological regulation and drug delivery strategies. Advanced drug delivery reviews, 173, 504–519. https://doi.org/10.1016/j.addr.2021.03.021
  6. Netala, V. R., Hou, T., Wang, Y., Zhang, Z., & Teertam, S. K. (2025). Cardiovascular Biomarkers: Tools for Precision Diagnosis and Prognosis. International journal of molecular sciences, 26(7), 3218. https://doi.org/10.3390/ijms26073218
  7. Nikolov, A., & Popovski, N. (2022). Extracellular Matrix in Heart Disease: Focus on Circulating Collagen Type I and III Derived Peptides as Biomarkers of Myocardial Fibrosis and Their Potential in the Prognosis of Heart Failure: A Concise Review. Metabolites, 12(4), 297. https://doi.org/10.3390/metabo12040297
  8. Ravassa, S., López, B., Treibel, T. A., San José, G., Losada-Fuentenebro, B., Tapia, L., Bayés-Genís, A., Díez, J., & González, A. (2023). Cardiac Fibrosis in heart failure: Focus on non-invasive diagnosis and emerging therapeutic strategies. Molecular aspects of medicine, 93, 101194. https://doi.org/10.1016/j.mam.2023.101194
  9. Shanavas, S., Ajas, M., Mohammed, A., Hameedh Mahamood, A., Wasim, A., Rahman Mohamed Elmohamed, A., Khan Mohammad, Z., Ahmad, A., Raveendran Prathapan, A., & Salman Arif, M. (2025). The Role of Cardiovascular Biomarkers in Early Detection of Myocardial Fibrosis. Cardiology and Cardiovascular Medicine, 9(3). https://doi.org/10.26502/fccm.92920431

 

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