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Organ crosstalk: the potent roles of inflammation and fibrotic changes in the course of organ interactions

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Abstract

Background

Organ crosstalk can be defined as the complex and mutual biological communication between distant organs mediated by signaling factors. Normally, crosstalk helps to coordinate and maintain homeostasis, but sudden or chronic dysfunction in any organ causes dysregulation in another organ. Many signal molecules, including cytokines and growth factors, are involved in the metabolic dysregulation, and excessive or inappropriate release of these molecules leads to organ dysfunction or disease (e.g., obesity, type 2 diabetes).

Aim and method

The aim of this review is to reveal the impact of organ crosstalk on the pathogenesis of diseases associated with organ interactions and the role of inflammatory and fibrotic changes in the organ dysfunction. After searching in MEDLINE, PubMed and Google Scholar databases using ‘organ crosstalk’ as a keyword, studies related to organ crosstalk and organ interaction were compiled and examined.

Conclusion

The organ crosstalk and the functional integration of organ systems are exceedingly complex processes. Organ crosstalk contributes to metabolic homeostasis and affects the inflammatory response, related pathways and fibrotic changes. As in the case of interactions between adipose tissue and intestine, stimulation of inflammatory mechanisms plays an active role in the development of diseases including insulin resistance, obesity, type 2 diabetes and hepatic steatosis. The increased level of knowledge about the ‘crosstalk’ between any organ and distant organs will facilitate the early diagnosis of the disease as well as the management of the treatment practices in the short- and long-term organ dysfunction.

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Abbreviations

AGEs:

Advanced glycation end products

AKI:

Acute kidney injury

ALI:

Acute lung injury

ANP:

Atrial natriuretic peptide

AP-1:

Activator protein 1

BNP:

B-type natriuretic peptide

CKD:

Chronic kidney disease

COX-2:

Cyclooxygenase-2

CVD:

Cardiovascular disease

CRP:

C-reactive protein

DAMPs:

Damage-associated molecular patterns

DM:

Diabetes mellitus

ECM:

Extracellular matrix

EMT:

Epithelial–mesenchymal transition

ER:

Endoplasmic reticulum

EVs:

Extracellular vesicles

FFA:

Free fatty acids

FGF:

Fibroblast growth factor

FXR:

Farnesoid × receptor

HFD:

High fat diet

HIF-1:

Hypoxia-inducible factor 1

IFN-γ:

Interferon gamma

IR:

Insulin resistance

IRI:

Ischemia/reperfusion injury

IL:

Interleukin

iNOS:

Inducible nitric oxide synthase

JNK:

c-Jun N-terminal kinase

KIM-1:

Kidney injury molecule 1

L-FABP:

Liver-type fatty acid-binding protein

LPS:

Lipopolysaccharides

MAPK:

Mitogen-activated protein kinase

MYD88:

Myeloid differentiation factor 88

NASH:

Non-alcoholic steatohepatitis

NAFLD:

Non-alcoholic fatty liver disease

NF-κB:

Nuclear factor kappa B

NGAL:

Neutrophil gelatinase associated lipocalin

NLRP3:

Nucleotide-binding domain 3

NO:

Nitric oxide

NRF2:

Nuclear factor erythroid 2-related factor 2

NT-proBNP:

N-terminal pro–B-type natriuretic peptide

MIF:

Macrophage migration inhibitory factor

MODS:

Multiple organ dysfunction syndrome

MOF:

Multiple organ failure

PAI-1:

Plasminogen activator inhibitor-1

PAMPs:

Pathogen-associated molecular patterns

PNPLA3:

Patatin-like phospholipase domain-containing 3

PI3:

Phosphatidylinositol 3-kinase

PPAR-γ:

Peroxisome proliferator-activated receptor-γ

ROS:

Reactive oxygen species

SCFAs:

Short change fatty acids

SIRS:

Systemic inflammatory response syndrome

sST2:

Soluble suppressor of tumorigenicity 2

STAT3:

Signal transducer and activator of transcription 3

TECs:

Tubular epithelial cells

TGF-β:

Transforming growth factor

TLR:

Toll-like receptor

TNF-α:

Tumor necrosis factor alpha

TNF-RII:

Tumor necrosis factor receptor II

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  1. Department of Biochemistry, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey

    Ferah Armutcu

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Armutcu, F. Organ crosstalk: the potent roles of inflammation and fibrotic changes in the course of organ interactions. Inflamm. Res. 68, 825–839 (2019). https://doi.org/10.1007/s00011-019-01271-7

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  • DOI: https://doi.org/10.1007/s00011-019-01271-7

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