Evidence map›Paper›PMID 19384726›Full record

ArticleMicrocirculation (New York, N.Y. : 1994)2009

2008 Landis Award lecture. Inflammation and the autodigestion hypothesis.

Geert W Schmid-Schönbein

Open access · greenAbstract readLecture
In one paragraph

Article in Microcirculation (New York, N.Y. : 1994), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Aging by autodigestion.PloS one · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. IGF-1 receptor cleavage in hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2018
    Article
  11. Article
  12. Observational
  13. Review
  14. Article
  15. Article
  16. Hyperthermia induces injury to the intestinal mucosa in the mouse: evidence for an oxidative stress mechanism.American journal of physiology. Regulatory, integrative and comparative physiology · 2012
    Article
  17. Article
  18. Article
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

1 author at 1 institution in 1 country.

Geert W Schmid-SchönbeinDepartment of Bioengineering, University of California-San Diego, La Jolla, California 92093-0412, USA. gwss@bioeng.ucsd.edu
University of California, San Diego · US

Funding

MOLECULAR BASIS OF ENDOTHELIAL MECHANICS AND ADHESIONP01HL043026 · NHLBI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SCHMID-SCHOENBEIN, GEERT W. · 1990 to 2005
$8.3M
STRUCTURE/FUNCTION OF THE MICROCIRCULATIOMR01HL010881 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SCHMID-SCHOENBEIN, GEERT W. · 1985 to 2011
$3.1M
Microvascular Injury and Pancreatic Enzyme ProductsR01HL067825 · NHLBI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SCHMID-SCHOENBEIN, GEERT W. · 2001 to 2005
$1.5M
Hemorrhagic Shock and Pancreatic Enzyme ProductsR01HL076180 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOYT, DAVID B. · 2004 to 2007
$1.4M
2006 Molecular Mechanisms in Lymphatic Function & Disease Gordon ConferenceR13HL084942 · NHLBI · GORDON RESEARCH CONFERENCES · PI SCHMID-SCHOENBEIN, GEERT W. · 2006 to 2006
$15k
NHLBI NIH HHS HL10881-42NHLBI NIH HHS HL67825NHLBI NIH HHS HL76180NHLBI NIH HHS P01 HL043026NHLBI NIH HHS R01 HL010881NHLBI NIH HHS R01 HL067825NHLBI NIH HHS R01 HL076180NHLBI NIH HHS R13 HL084942
6 · The paper itself

Abstract

Although long recognized in microvascular research, an increasing body of evidence suggests that inflammatory markers are present in human diseases. Since the inflammatory cascade serves as a repair mechanism, the presence of inflammatory markers in patient groups has raised an important question about the mechanisms that initiate the inflammatory cascade (i.e., the mechanisms that cause tissue injury). Using a severe form of inflammation, shock, and multiorgan failure, for which there is no accepted injury mechanism, we summarize studies that suggest that the powerful pancreatic digestive enzymes play a central role in the destruction of the intestine and other tissues if their compartmentalization in the lumen of the intestine and in the pancreas is compromised. Further, we summarize evidence that uncontrolled degrading enzyme activity in plasma causes proteolytic cleavage of the extracellular domain of membrane receptors and loss of associated cell functions. For example, in a model of metabolic disease with type II diabetes, proteolytic cleavage of the insulin receptor causes the inability of insulin to signal glucose transport across membranes. The evidence suggests that uncontrolled proteolytic and lipolytic enzyme activity may trigger the mechanism for tissue injury. The significance of such mechanisms remain to be explored in human diseases.

Indexed as

BiomarkersHumansInflammationIntestinesMatrix MetalloproteinasesPancreasBiomarkersMatrix Metalloproteinases

Identifiers

PMID19384726
PMCPMC2677689
OpenAlexW1965759325

What OpenQuestion 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 OpenQuestion graph.