Systems biology in inflammatory bowel diseases

Polytarchou, Christos; Κούκος, Γεώργιος; Iliopoulos, Dimitrios

doi:10.1097/mog.0000000000000081

Cited by 33 publications

(20 citation statements)

References 92 publications

(89 reference statements)

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“…Mucosal changes in colitis are characterized by ulcerative lesions accompanied by prominent inflammatory infiltrates in the bowel wall (Polytarchou et al 2014). Mesalamine (5-aminosalicylic acid) is the first-line therapy for colitis.…”

Section: Colitismentioning

confidence: 99%

H2S and Inflammation: An Overview

Bhatia

2015

Handbook of Experimental Pharmacology

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Inflammation is a response to traumatic, infectious, post-ischemic, toxic, or autoimmune injury. However, uncontrolled inflammation can lead to disease, and inflammation is now believed to be responsible for several disease conditions. Research in our laboratory has shown that hydrogen sulfide (H2S) acts as a novel mediator of inflammation. At present, work in several research groups worldwide is focused on determining the role of H2S in inflammation. H2S has been implicated in different inflammatory conditions. Most of this research involved working with animal models of disease and in vitro systems. Recent research, however, points to a role of H2S in clinical inflammatory disease as well. This chapter describes our current understanding of the role of H2S in inflammation.

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Section: Colitismentioning

confidence: 99%

H2S and Inflammation: An Overview

Bhatia

2015

Handbook of Experimental Pharmacology

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“…Nevertheless, we underscore that identifying functional connectors of distinct diseases will help clinicians and drug and biotechnology developers to target the same biomarker in the development of novel approaches for early disease diagnosis or treatment. There is already a veritable trend to apply systems biology to identify central regulators in the IBD interactome (Polytarchou et al, 2014;Sun et al, 2014), which can be easily transferred to Crohn's disease and periodontitis, at the same time, thus increasing clinical benefits while decreasing the long-term costs significantly.…”

Section: Discussionmentioning

confidence: 99%

Two Cheers for Crohn's Disease and Periodontitis: Beta-Defensin-2 as an Actionable Target to Intervene on Two Clinically Distinct Diseases

Keskin

Zeidán-Chuliá

Gürsoy

et al. 2015

OMICS: A Journal of Integrative Biology

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Recent advances in multi-omics approaches encompassing genomics, transcriptomics, proteomics, and metabolomics offer hitherto unprecedented insights on common complex human diseases. A unique angle pertinent for both diagnostic and therapeutic sciences involves rethinking clinically distinct diseases with a view to their shared molecular targets, interactomes, and pathophysiologies. Reflecting at a scale of disease-to-disease associations might help clinicians, public health practitioners, drug and biotechnology developers, and associated knowledge industries in the current era. This review article examines the hypothesis that "Intersecting Molecular Pathways Permit Interventions on Multiple Clinical Endpoints", thus uniquely bringing together Crohn's disease and periodontitis. Furthermore, we propose a novel connector molecular target between these two ostensibly distinct diseases at a clinical level, human beta defensin (hBD)-2, and suggest pathways by which hBD-2 can conceivably connect Crohn's disease and periodontitis by virtue of regulating the innate-immune response. We conclude by emphasizing different approaches where hBD-2 can be employed as a diagnostic and therapeutic tool to improve the quality of life of susceptible individuals and minimize the economic costs of these two major global public health problems. The strategy presented here also presents potentials for targeting of multiple diseases through a unique "nodal molecular target" that "speaks to" multiple clinical endpoints.

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“…Each of them represents a 'node' connected to the other nodes of the same category in the network through positive or negative interactions called 'edges'. The higher the number of edges coming from or going to any particular node, the higher is the control that this node exerts on the whole network [18] . The node that has the highest number of edges is then considered the 'central regulator' or 'hub' of the network and becomes the logical and likely the best target to modulate the whole network.…”

Section: How To Personalize Medicine?mentioning

confidence: 99%

“…2 ). The simple numerical multiplication of these data makes for a staggering number of possible interactions and nodes, but the current technology that is available enables the identification of such interactions and uncovering the key regulators that will then become the targets for intervention [18] . For instance, an IBD patient whose pathogenic networks are dominated by microbiome and immune nodes will need therapeutic interventions that do not involve behavioral (exposome) or genomic modifications; another IBD patient whose pathogenic networks are dominated by exposome and immune nodes will need therapeutic interventions that do not involve microbial or genomic modifications.…”

Section: Why Personalize Medicine In Ibd?mentioning

confidence: 99%

Tailoring Treatment to the Individual Patient - Will Inflammatory Bowel Disease Medicine Be Personalized?

Fiocchi¹

2015

Dig Dis

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Personalized medicine is variably defined as a new system aimed at providing optimal medical care by using comprehensive pathophysiology-based information on all aspects and components of a disease process to prevent, diagnose and treat in ways that are custom-made for the individual patient. The need for personalized medicine derives from the realization that today's most challenging medical conditions are chronic complex diseases with multiple pathogenic components that interact with each other. Complexity and interaction together create unique molecular pathways that are only relevant to certain disease subtypes, but not to the entire population of patients with the same diagnosis. Thus, complex diseases cannot be properly controlled, and much less cured, by modulating single components at sporadic time points in the course of the disease or administering the same treatment to all patients, as we currently do in the management of inflammatory bowel disease (IBD). The implementation of personalized medicine requires entirely novel and methodologically sophisticated bioinformatics-based approaches that use comprehensive and detailed information on the various components (‘omes') of the disease process. This requires identifying the key controllers (‘hubs') of pathogenic pathways in a totally unbiased fashion and discovering highly specific agents that can selectively block or even revert pathogenic events. IBD is a perfect example of a condition with multiple causes and multiple mechanisms, and IBD patients will unquestionably benefit from the adoption of personalized medicine in the near future.

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Systems biology in inflammatory bowel diseases

Cited by 33 publications

References 92 publications

H2S and Inflammation: An Overview

H2S and Inflammation: An Overview

Two Cheers for Crohn's Disease and Periodontitis: Beta-Defensin-2 as an Actionable Target to Intervene on Two Clinically Distinct Diseases

Tailoring Treatment to the Individual Patient - Will Inflammatory Bowel Disease Medicine Be Personalized?

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