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Review
. 2020 Aug 4;21(15):5568.
doi: 10.3390/ijms21155568.

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

Elena Vianello  1 , Marta Kalousová  2 , Elena Dozio  1 , Lorenza Tacchini  1 , Tomáš Zima  2 , Massimiliano Marco Corsi Romanelli  1   3
Affiliations
Review

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

Elena Vianello et al. Int J Mol Sci. .

Abstract

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.

Keywords: cardiovascular diseases (CVDs); chronic kidney disease (CKD); obesity; osteopontin (OPN); renal disorders; visceral adipose tissue (VAT).

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Cardiac fibro-adipocyte progenitor (FAP) activation in the heart: multipotent fibro-adipocyte progenitors (FAPs) are a stem reserve of the quiescent cells present in the heart, ready to be activated during heart injury. Normally, FAPs protect the myocardium by repairing lesions. Moreover, under chronic heart stresses, such as pressure overload, hypertrophy and cardiomyocyte injury, the quiescent FAPs become activated and differentiated in two non-cardiac lineages. Becoming intra-cardiac adipocytes, they release adipose mediators involved in heart inflammation, whereas becoming new intra-cardiac fibroblasts, they intervene in local collagen deposition and scar formation. Interestingly, both maturated lineages promote macrophage recruitment and activation, although no studies have underlined the possible involvement of osteopontin (OPN) in FAP activation and maturation.
Figure 2
Figure 2
Summary diagram illustrating the role of OPN in mediating cardiac and renal disorders in the presence of obesity.
See this image and copyright information in PMC

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