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Biomarkers in Cardiovascular Diseases: Diagnosis, Pathology and Treatment

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 January 2026 | Viewed by 2103

Special Issue Editor


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Guest Editor
Department of Cardiovascular Sciences, Policlinico Umberto I, Sapienza Università di Roma, 00185 Rome, Italy
Interests: cardiology; arrhythmia; heart failure; coronary artery dissection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are one of the main causes of morbidity and mortality worldwide, destined to increase their diffusion due to the aging of the world population. Biomarker assessment represents a cornerstone for the diagnostic and prognostic assessment of patients with cardiovascular diseases. However, in order to improve the management of these conditions, it is important to identify new molecular biomarkers reflecting new pathophysiological pathways involved in cardiovascular diseases.

In heart failure, the leading biomarkers used either in diagnosis or prognostic evaluation are natriuretic peptides released from cardiomyocytes in response to parietal stretch. Beyond this, there are other interesting and promising biomarkers, such as sST-2 or galectine-3, respectively, an interleukin receptor and a regulator of fibrosis development, which have been shown to be predictors of mortality and new onset of HF. Moreover, high-sensitivity troponins are useful biomarkers in several cardiovascular conditions. In myocardial infarction, their release is due to cardiomyocyte necrosis. Different studies have shown how progressive cardiomyocyte injury has also been demonstrated to be predictive of cardiovascular events in HF. Other biomarkers reflecting alternative pathophysiological pathways are under study. In particular, C-reactive protein, IL-6, fibrinogen and TNF-α are the biomarkers of inflammation, while isoprostane is a marker of oxidative stress.

To better highlight the recent advances, this Special Issue will focus on findings regarding new biomarkers in cardiovascular diseases, as well as innovative use of the already-known biomarkers that may help in patient management.

Specifically, original articles reporting new results or reviews of the current literature on this aspect will be taken into account. The Special Issue wants to focus on basic research (clinical studies are excluded from the scope of this Special Issue) to produce a more complete comprehension of the role of biomarkers in diagnostic, pathology and therapeutic guidance in cardiovascular diseases.

Dr. Marco Valerio Mariani
Guest Editor

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Keywords

  • heart failure
  • myocardial remodeling
  • ischemic heart disease
  • myocarditis
  • cardiomyopathies
  • prevention
  • diagnosis
  • therapy

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Published Papers (2 papers)

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Research

13 pages, 681 KB  
Article
Short-term effects of DAPAgliflozin on Lung fUNction, sleep apneas, and circulatinG surfactant protein B in Heart Failure with reduced ejection fraction (DAPA-LUNG-HF)
by Massimo Mapelli, Irene Mattavelli, Elisabetta Salvioni, Cristina Banfi, Alice Mallia, Arianna Galotta, Valentina Mantegazza, Anna Garlaschè, Jeness Campodonico, Filippo Maria Rubbo, Chiara Paganin, Teresa Maria Capovilla, Rebecca Caputo, Mauro Contini, Paola Gugliandolo, Carlo Vignati, Beatrice Pezzuto, Giulia Grilli, Marco Scatigna, Alice Bonomi, Gianfranco Sinagra, Manuela Muratori and Piergiuseppe Agostoniadd Show full author list remove Hide full author list
Int. J. Mol. Sci. 2025, 26(16), 7696; https://doi.org/10.3390/ijms26167696 - 8 Aug 2025
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Abstract
The mechanisms underlying the effects of dapagliflozin in heart failure with reduced ejection fraction (HFrEF) are not yet fully understood. This study aims to evaluate the effect of the drug on cardiorespiratory function by assessing alveolar–capillary membrane characteristics, sleep apnea, pulmonary and cardiac [...] Read more.
The mechanisms underlying the effects of dapagliflozin in heart failure with reduced ejection fraction (HFrEF) are not yet fully understood. This study aims to evaluate the effect of the drug on cardiorespiratory function by assessing alveolar–capillary membrane characteristics, sleep apnea, pulmonary and cardiac performance in stable HFrEF patients. Seventy-three patients with stable HFrEF were enrolled, with 66 completing the six-month follow-up. Analyses included assessment of the alveolar–capillary membrane by diffusion capacity, including its membrane diffusion and capillary volume components and measurements of proSP-B in the blood, an emerging biomarker of alveolar–capillary membrane function. Pulmonary function tests, overnight respiratory monitoring, and echocardiographic parameter collection were also conducted. After 6 months, a reduction in circulating proSP-B levels was observed (32.65 ± 13.36 at baseline vs. 30.86 ± 12.45 AU at 6 months, p for trend 0.0092), accompanied by improvements in echocardiographic parameters (left ventricle ejection fraction and pulmonary pressures). Pulmonary function tests and overnight respiratory monitoring showed no significant changes in lung diffusion, spirometry, or obstructive sleep apnea (apnea hypopnea index from 5.0 [1.1–16.6] at baseline to 6.2 [0.7–13.8]/h; p = n.s.). A significant reduction in central sleep apnea (CSA) was noted in the 13 patients with at least one CSA at baseline (15 [3–48] vs. 0 [0–18.5]/h, p = 0.017). Dapagliflozin demonstrates both hemodynamic and non-hemodynamic effects, particularly improving alveolar–capillary membrane function. This study highlights the multifactorial benefits of dapagliflozin in patients with stable HFrEF and the potential of proSP-B as a sensitive marker for evaluating therapeutic response. Full article
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12 pages, 1583 KB  
Article
Influence of Anticoagulants on the Dissociation of Cardiac Troponin Complex in Blood Samples
by Natalia S. Riabkova, Alexander E. Kogan, Ivan A. Katrukha, Alexandra V. Vylegzhanina, Agnessa P. Bogomolova, Amina K. Alieva, Dmitry V. Pevzner, Anastasia V. Bereznikova and Alexey G. Katrukha
Int. J. Mol. Sci. 2024, 25(16), 8919; https://doi.org/10.3390/ijms25168919 - 16 Aug 2024
Cited by 3 | Viewed by 1395
Abstract
Immunodetection of cardiac isoforms of troponin I (cTnI) and troponin T (cTnT) in blood samples is widely used for the diagnosis of acute myocardial infarction. The cardiac troponin complex (ITC-complex), comprising cTnI, cTnT, and troponin C (TnC), makes up a large portion of [...] Read more.
Immunodetection of cardiac isoforms of troponin I (cTnI) and troponin T (cTnT) in blood samples is widely used for the diagnosis of acute myocardial infarction. The cardiac troponin complex (ITC-complex), comprising cTnI, cTnT, and troponin C (TnC), makes up a large portion of troponins released into the bloodstream after the necrosis of cardiomyocytes. However, the stability of the ITC-complex has not been fully investigated. This study aimed to investigate the stability of the ITC-complex in blood samples. A native ITC-complex was incubated in buffer solutions, serum, and citrate, heparin, or EDTA plasma at various temperatures. Western blotting and gel filtration were performed, and troponins were detected using specific monoclonal antibodies. The ITC-complex dissociated at 37 °C in buffers with or without anticoagulants, in citrate, heparin, and EDTA plasmas, and in serum, into a binary cTnI-TnC complex (IC-complex) and free cTnT. In plasma containing heparin and EDTA, the IC-complex further dissociated into free TnC and cTnI. No dissociation was found at 4 °C or at room temperature (RT) in all matrices within 24 h except for EDTA plasma. After incubation at 37 °C in EDTA plasma and serum, dissociation was accompanied by proteolytic degradation of both cTnI and cTnT. The presence of anti-troponin autoantibodies in the sample impeded dissociation of the ITC-complex. The ITC-complex dissociates in vitro to form the IC-complex and free cTnT at 37 °C but is mostly stable at 4 °C or RT. Further dissociation of the IC-complex occurs at 37 °C in plasmas containing heparin and EDTA. Full article
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