Corrigendum to “Chemokines and heart disease: A network connecting cardiovascular biology to immune and autonomic nervous systems” (Mediators Inflamm (2016) 2016, (5902947) DOI: 10.1155/2016/5902947

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Corrigendum

Corrigendum to

“Chemokines and Heart Disease: A Network

Connecting Cardiovascular Biology to Immune and Autonomic

Nervous Systems

”

Veronica Dusi,

1

Alice Ghidoni,

2,3

Alice Ravera,

4

Gaetano M. De Ferrari,

1,3

and Laura Calvillo

2

1_{Department of Cardiology and Cardiovascular Clinical Research Center, Fondazione IRCCS Policlinico San Matteo,}

27100 Pavia, Italy

2_{Center for Cardiac Arrhythmias of Genetic Origin, IRCCS Istituto Auxologico Italiano, 20095 Milan, Italy} 3_{Department of Molecular Medicine, University of Pavia, 27100 Pavia, Italy}

4_{Institute of Cardiology, Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health,}

University and Civil Hospital of Brescia, 25123 Brescia, Italy

Correspondence should be addressed to Laura Calvillo; [email protected] Received 13 December 2017; Accepted 18 December 2017; Published 10 January 2018

Copyright © 2018 Veronica Dusi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

In the article titled

“Chemokines and Heart Disease: A

Network Connecting Cardiovascular Biology to Immune

and Autonomic Nervous Systems

” [1], there was an error

in Figure 2. The corrected

ﬁgure is shown below.

Hindawi

Mediators of Inﬂammation

Volume 2018, Article ID 4128049, 2 pages https://doi.org/10.1155/2018/4128049

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References

[1] V. Dusi, A. Ghidoni, A. Ravera, G. M. De Ferrari, and L. Calvillo, “Chemokines and heart disease: a network con-necting cardiovascular biology to immune and autonomic nervous systems,” Mediators of Inﬂammation, vol. 2016, Article ID 5902947, 16 pages, 2016.

Ischemia pH

Ionic pump damage (H+_/Na+_{and Na}+_/Ca+₎

No reperfusion

CCL5

CCL2

BRIEF Is-Rep cycles

ROS

Reperfusion (Rep)

IL-6 CXCL8, CCL2, CCL11

PMN and monocyte recruitement Cytokine production Modulation of macrophage function

PMN-dependent myocyte injury

Macrophage infiltration

Repair processes, angiogenesis Protective survival

pathway

Increased leukocyte infiltration

Infarct size increase remodeling repair

or heart failure

NF-휅b, c-Fos, c-Jun activation Possible angiogenesis Macrophages infiltration_–

collagen increase–repair– remodeling–LV dysfunction CXCL1-CCL2

CXCL3-4, CXCL2 CXCL2

Membrane cell rupture

Adenosine ROS Mast cell Histamine P-selectin TNF Rolling of leukocytes along the inner

surface of the vessel wall

Possible evolution...

C1q C5a

↑ ↑

Figure 2: Metabolic changes triggered by ischemic insult and possible evolutions of the injury with the crosstalk between chemokines. The pH decrease, provoked by ischemia, is the event turning on the process. The cell membrane is damaged and debris activates the classic complement pathway in the infarcted myocardium. ROS, adenosine, and complement activate mast cells to produce TNF and histamine, leading to leukocyte recruitment from the vessels. Depending on the presence or the absence of reperfusion, there is a diﬀerent crosstalk between chemokines aimed at restoring the balance. Dysregulated or exaggerated responses may actually lead to a progression of the disease (see text for details, chemokines in red).