Utility of temporal profiles of new cardio-renal and pulmonary candidate biomarkers in chronic heart failure

Branković, Miloš; Akkerhuis, K. Martijn; Mouthaan, Henk; Constantinescu, Alina A.; Çalışkan, Kadir; Ramshorst, Jan van; Germans, Tjeerd; Umans, Victor; Kardys, Isabella

doi:10.1016/j.ijcard.2018.08.001

Cited by 25 publications

(22 citation statements)

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“…A new study by Brankovic et al (52) examined the potential of SP-D as a biomarker in patients with chronic heart failure. Brankovic et al (52) reported that SP-D was associated with a worsened clinical outcome (worsened heart failure, heart transplantation, death to CVD) independently of the patient's clinical profile and pharmacological treatment during the follow-up period.…”

Section: Sp-d Variation In Clinical Studiesmentioning

confidence: 99%

The Dual Role of Surfactant Protein-D in Vascular Inflammation and Development of Cardiovascular Disease

2019

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Cardiovascular disease (CVD) is responsible for 31% of all global deaths. Atherosclerosis is the major cause of cardiovascular disease and is a chronic inflammatory disorder in the arteries. Atherosclerosis is characterized by the accumulation of cholesterol, extracellular matrix, and immune cells in the vascular wall. Recently, the collectin surfactant protein-D (SP-D), an important regulator of the pulmonary immune response, was found to be expressed in the vasculature. Several in vitro studies have examined the role of SP-D in the vascular inflammation leading to atherosclerosis. These studies show that SP-D plays a dual role in the development of atherosclerosis. In general, SP-D shows anti-inflammatory properties, and dampens local inflammation in the vessel, as well as systemic inflammation. However, SP-D can also exert a pro-inflammatory role, as it stimulates C-C chemokine receptor 2 inflammatory blood monocytes to secrete tumor necrosis-factor α and increases secretion of interferon-γ from natural killer cells. In vivo studies examining the role of SP-D in the development of atherosclerosis agree that SP-D plays a proatherogenic role, with SP-D knockout mice having smaller atherosclerotic plaque areas, which might be caused by a decreased systemic inflammation. Clinical studies examining the association between SP-D and cardiovascular disease have reported a positive association between circulatory SP-D level, carotid intima-media thickness, and coronary artery calcification. Other studies have found that circulatory SP-D is correlated with increased risk of both total and cardiovascular disease mortality. Both in vitro, in vivo, and clinical studies examining the relationship between SP-D and CVDs will be discussed in this review.

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Section: Sp-d Variation In Clinical Studiesmentioning

confidence: 99%

The Dual Role of Surfactant Protein-D in Vascular Inflammation and Development of Cardiovascular Disease

2019

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“…M2 (CD14++CD16++) macrophages are responsible for wound healing, neovascularization, and myofibroblast activation. Their profibrotic action within the myocardium is mediated by osteopontin, which we found to be associated with adverse clinical outcome in our previous investigation . The levels of M2 macrophages are increased in asymptomatic diastolic dysfunction, heart failure with preserved ejection fraction, and HF with reduced ejection fraction .…”

Section: Discussionmentioning

confidence: 59%

“…The current analysis specifically includes biomarkers related to the action of two cellular players of the innate immune system: macrophages and, to a lesser extent, neutrophils. We describe cytokines and chemokines elsewhere; moreover, we assigned those molecules that, besides their function in the innate immunity, play important roles in other processes, to the pathways listed above; such as for example galectin‐3 or suppression of tumorigenicity 2 . Here, we aim for a deeper understanding of innate immune system dynamics in patients with heart failure and to investigate the utility of macrophage‐ and neutrophil‐related molecules as biomarkers of prognosis in these patients.…”

Section: Introductionmentioning

confidence: 99%

Temporal patterns of macrophage‐ and neutrophil‐related markers are associated with clinical outcome in heart failure patients

et al. 2020

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Aims Evidence on the association of macrophage-and neutrophil-related blood biomarkers with clinical outcome in heart failure patients is limited, and, with the exception of C-reactive protein, no data exist on their temporal evolution. We aimed to investigate whether temporal patterns of these biomarkers are related to clinical outcome in patients with stable chronic heart failure (CHF). Methods and ResultsIn 263 patients with CHF, we performed serial plasma measurements of scavenger receptor cysteine-rich type 1 protein M130 (CD163), tartrate-resistant acid phosphatase type 5 (TRAP), granulins (GRN), spondin-1 (SPON1), peptidoglycan recognition protein 1 (PGLYRP1), and tissue factor pathway inhibitor (TFPI). The Cardiovascular Panel III (Olink Proteomics AB, Uppsala, Sweden) was used. During 2.2 years of follow-up, we collected 1984 samples before the occurrence of the composite primary endpoint (PE) or censoring. For efficiency, we selected 567 samples for the measurements (all baseline samples, the last two samples preceding the PE, and the last sample before censoring in event-free patients). The relationship between repeatedly measured biomarker levels and the PE was evaluated by joint models. Mean (±standard deviation) age was 67 ± 13 years; 189 (72%) were men; left ventricular ejection fraction (%) was 32 ± 11. During follow-up, 70 (27%) patients experienced the PE. Serially measured biomarkers predicted the PE in a multivariable model adjusted for baseline clinical characteristics [hazard ratio (95% confidence interval) per 1-standard deviation change in biomarker]: CD163 [2.07(1.47-2.98), P < 0.001], TRAP [0.62 (0.43-0.90), P = 0.009], GRN [2.46 (1.64-3.84), P < 0.001], SPON1 [3.94 (2.50-6.50), P < 0.001], and PGLYRP1 [1.62 (1.14-2.31), P = 0.006].Conclusions Changes in plasma levels of CD163, TRAP, GRN, SPON1, and PGLYRP1 precede adverse cardiovascular events in patients with CHF.

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“…Indeed, OPN physiologically regulates the developmental processes, local tissue remodeling and healing, as well as the senescence in adipocytes, cardiac and renal cells [26]. On the contrary, the aberrant expression of OPN is directly associated with obesity-related disorders, such as type 2 diabetes, cardiac and renal dysfunctions [20,34]. Moreover, it is reported that the upregulation of OPN expression in immune systems leads to worsening of chronic inflammatory conditions, including atherosclerosis and vascular dysfunction [34].…”

Section: Osteopontin (Opn) Structure and Physiological Functionsmentioning

confidence: 99%

“…Due to the multifunctional properties of OPN and its ubiquitous expression in the body, its pivotal role in coexistent disorders like obesity, renal dysfunctions and cardiovascular diseases (CVDs) is currently debated [15,16], in which simultaneous etiologic factors can promote OPN signaling deregulation and aggravate the cross-disorders, like cardiac or renal-fat diseases [15][16][17]. Indeed, it is notable that the main common factor highlighted as a promoter of the progression and development of cardiovascular and renal disorders is the increase in visceral fat mass [18][19][20]. Visceral adipose tissue (VAT), which extends during overweight and obesity, is associated not only with the development of type 2 diabetes or hypertension, but also it is recognized as a well-known risk factor for heart failure (HF), coronary artery diseases, valve diseases and for all main events associated with the loss of renal functions [21,22].…”

Section: Introductionmentioning

confidence: 99%

Osteopontin: The Molecular Bridge between Fat and Cardiac–Renal Disorders

Vianello

Kalousová

Dozio

et al. 2020

IJMS

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Osteopontin (OPN) is a multifaceted matricellular protein, with well-recognized roles in both the physiological and pathological processes in the body. OPN is expressed in the main organs and cell types, in which it induces different biological actions. During physiological conditioning, OPN acts as both an intracellular protein and soluble excreted cytokine, regulating tissue remodeling and immune-infiltrate in adipose tissue the heart and the kidney. In contrast, the increased expression of OPN has been correlated with the severity of the cardiovascular and renal outcomes associated with obesity. Indeed, OPN expression is at the “cross roads” of visceral fat extension, cardiovascular diseases (CVDs) and renal disorders, in which OPN orchestrates the molecular interactions, leading to chronic low-grade inflammation. The common factor associated with OPN overexpression in adipose, cardiac and renal tissues seems attributable to the concomitant increase in visceral fat size and the increase in infiltrated OPN+ macrophages. This review underlines the current knowledge on the molecular interactions between obesity and the cardiac–renal disorders ruled by OPN.

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Utility of temporal profiles of new cardio-renal and pulmonary candidate biomarkers in chronic heart failure

Cited by 25 publications

References 50 publications

The Dual Role of Surfactant Protein-D in Vascular Inflammation and Development of Cardiovascular Disease

The Dual Role of Surfactant Protein-D in Vascular Inflammation and Development of Cardiovascular Disease

Temporal patterns of macrophage‐ and neutrophil‐related markers are associated with clinical outcome in heart failure patients

Osteopontin: The Molecular Bridge between Fat and Cardiac–Renal Disorders

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