Evidence map›Paper›PMID 27303926›Full record

ReviewMolecular bioSystems2016

Molecular and genetic inflammation networks in major human diseases.

Yongzhong Zhao, Christian V Forst, Camil E Sayegh, I-Ming Wang, Xia Yang, Bin Zhang

Open access · greenAbstract readReview
In one paragraph

Review in Molecular bioSystems, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 67 citations in OpenAlex.

  1. Trial
  2. Article
  3. A comprehensive review of the effects ofJournal of ginseng research · 2025
    Review
  4. Article
  5. Article
  6. New Molecular Mechanisms and Markers in Inflammatory Disorders.International journal of molecular sciences · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Clinical perspectives on the age-related increase of immunosuppressive activity.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  14. Variants in PRKCE and KLC1, Potential Regulators of Type I Psoriasis.Clinical, cosmetic and investigational dermatology · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Epigenetic Mechanisms of Inflammasome Regulation.International journal of molecular sciences · 2020
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 5 institutions in 4 countries.

Yongzhong ZhaoDepartment of Genetics and Genomic Sciences, Mount Sinai School of Medicine, 1425 Madison Avenue, NY 10029, USA. bin.zhang@mssm.edu and Institute of Genomics and Multiscale Biology, Mount Sinai School of Medicine, 1425 Madison Avenue, NY 10029, USA.
Christian V ForstDepartment of Genetics and Genomic Sciences, Mount Sinai School of Medicine, 1425 Madison Avenue, NY 10029, USA. bin.zhang@mssm.edu and Institute of Genomics and Multiscale Biology, Mount Sinai School of Medicine, 1425 Madison Avenue, NY 10029, USA.
Camil E SayeghVertex Pharmaceuticals (Canada) Incorporated, 275 Armand-Frappier, Laval, Quebec H7V 4A7, Canada.
I-Ming WangInformatics and Analysis, Merck Research Laboratories, Merck & Co., Inc., 770 Sumneytown Pike, West Point, PA 19486, USA. i_ming_wang@merck.com.
Xia YangDepartment of Integrative Biology and Physiology, University of California, Los Angeles, CA 90025, USA. xyang123@ucla.edu.
Bin ZhangDepartment of Genetics and Genomic Sciences, Mount Sinai School of Medicine, 1425 Madison Avenue, NY 10029, USA. bin.zhang@mssm.edu and Institute of Genomics and Multiscale Biology, Mount Sinai School of Medicine, 1425 Madison Avenue, NY 10029, USA.
Icahn School of Medicine at Mount Sinai · USGenomics (United Kingdom) · GBLaval Mayenne Technopole · FRUnited States Military Academy · USUniversity of California System · US

Funding

Integrative Network Biology Approaches to Identify, Characterize and Validate Molecular Subtypes in Alzheimer's DiseaseU01AG046170 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI WANG, MINGHUI, ZHANG, BIN · 2013 to 2022
$26.0M
Omics-Based Predictive Modeling of Age-Dependent Outcome to Influenza InfectionU01AI111598 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GHEDIN, ELODIE · 2013 to 2017
$13.3M
Lung Adenocarcinoma Invasion GenomicsR01CA163772 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MASSION, PIERRE P., POWELL, CHARLES A. · 2013 to 2017
$2.9M
NCI NIH HHS R01 CA163772NIAID NIH HHS U01 AI111598NIA NIH HHS U01 AG046170
6 · The paper itself

Abstract

It has been well-recognized that inflammation alongside tissue repair and damage maintaining tissue homeostasis determines the initiation and progression of complex diseases. Albeit with the accomplishment of having captured the most critical inflammation-involved molecules, genetic susceptibilities, epigenetic factors, and environmental factors, our schemata on the role of inflammation in complex diseases remain largely patchy, in part due to the success of reductionism in terms of research methodology per se. Omics data alongside the advances in data integration technologies have enabled reconstruction of molecular and genetic inflammation networks which shed light on the underlying pathophysiology of complex diseases or clinical conditions. Given the proven beneficial role of anti-inflammation in coronary heart disease as well as other complex diseases and immunotherapy as a revolutionary transition in oncology, it becomes timely to review our current understanding of the molecular and genetic inflammation networks underlying major human diseases. In this review, we first briefly discuss the complexity of infectious diseases and then highlight recently uncovered molecular and genetic inflammation networks in other major human diseases including obesity, type II diabetes, coronary heart disease, late onset Alzheimer's disease, Parkinson's disease, and sporadic cancer. The commonality and specificity of these molecular networks are addressed in the context of genetics based on genome-wide association study (GWAS). The double-sword role of inflammation, such as how the aberrant type 1 and/or type 2 immunity leads to chronic and severe clinical conditions, remains open in terms of the inflammasome and the core inflammatome network features. Increasingly available large Omics and clinical data in tandem with systems biology approaches have offered an exciting yet challenging opportunity toward reconstruction of more comprehensive and dynamic molecular and genetic inflammation networks, which hold great promise in transiting network snapshots to video-style multi-scale interplays of disease mechanisms, in turn leading to effective clinical intervention.

Indexed as

Gene Regulatory NetworksGenetic Association StudiesGenetic Predisposition to DiseaseAnimalsHost-Pathogen InteractionsHumansImmunity, InnateInflammationMice

Identifiers

PMID27303926
PMCPMC4955784
OpenAlexW2442594711

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.