Evidence map›Paper›PMID 19233238›Full record

ReviewAdvanced drug delivery reviews2009

Antioxidant enzyme gene transfer for ischemic diseases.

Jian Wu, James G Hecker, Nipavan Chiamvimonvat

Open access · greenAbstract readReview
In one paragraph

Review in Advanced drug delivery reviews, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.6field-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

24 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Protective Effects of L-Malate against Myocardial Ischemia/Reperfusion Injury in Rats.Evidence-based complementary and alternative medicine : eCAM · 2016
    Article
  12. Article
  13. Transduced PEP-1-heme oxygenase-1 fusion protein reduces remote organ injury induced by intestinal ischemia/reperfusion.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  14. Review
  15. Article
  16. Oxidative stress and antioxidant therapy in traumatic spinal cord injuries.Romanian journal of anaesthesia and intensive care · 2014
    Article
  17. Article
  18. Article
  19. Mitochondria and reactive oxygen species: physiology and pathophysiology.International journal of molecular sciences · 2013
    Article
  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

3 authors at 3 institutions in 1 country.

Jian WuDepartment of Internal Medicine, Transplant Research Program, University of California, Davis Medical Center, Sacramento, CA 95817, USA. jdwu@ucdavis.edu
James G Hecker
Nipavan Chiamvimonvat
California University of Pennsylvania · USUniversity of California Davis Medical Center · USVA Northern California Health Care System · US

Funding

Functional Interactions of Cardiac Ion ChannelsR01HL085844 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2007 to 2025
$7.3M
Translational Study of Cardiac DysfunctionR01HL085727 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN, SIRISH, PADMINI · 2008 to 2022
$5.7M
Non-viral controllable gene delivery for neuroprotectionR01NS046591 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HECKER, JAMES GORDON · 2003 to 2007
$1.7M
Functions of calcium-activated ion channels in the heartR01HL075274 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2004 to 2007
$1.5M
NONVIRAL GENE TRANSFER FOR CNS NEUROPROTECTIONK08NS001960 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HECKER, JAMES GORDON · 1999 to 2003
$550k
Anti-oxidative gene therapy for liver transplantationR21DK069939 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI WU, JIAN · 2005 to 2006
$294k
Regulation of ion channels in the heartI01BX000576 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI CHIAMVIMONVAT, NIPAVAN · 2009 to 2019
–
BLRD VA I01 BX000576NHLBI NIH HHS HL75274NHLBI NIH HHS HL85727NHLBI NIH HHS HL85844NHLBI NIH HHS R01 HL075274NHLBI NIH HHS R01 HL085727NHLBI NIH HHS R01 HL085844NIDDK NIH HHS DK069939NIDDK NIH HHS R21 DK069939NINDS NIH HHS K08 NS001960NINDS NIH HHS NS046591NINDS NIH HHS NS1960NINDS NIH HHS R01 NS046591
6 · The paper itself

Abstract

The balance of redox is pivotal for normal function and integrity of tissues. Ischemic insults occur as results of a variety of conditions, leading to an accumulation of reactive oxygen species (ROS) and an imbalanced redox status in the tissues. The oxidant stress may activate signaling mechanisms provoking more toxic events, and eventually cause tissue damage. Therefore, treatments with antioxidants, free radical scavengers and their mimetics, as well as gene transfer approaches to overexpress antioxidant genes represent potential therapeutic options to correct the redox imbalance. Among them, antioxidant gene transfer may enhance the production of antioxidant scavengers, and has been employed to experimentally prevent or treat ischemic injury in cardiovascular, pulmonary, hepatic, intestinal, central nervous or other systems in animal models. With improvements in vector systems and delivery approaches, innovative antioxidant gene therapy has conferred better outcomes for myocardial infarction, reduced restenosis after coronary angioplasty, improved the quality and function of liver grafts, as well as outcome of intestinal and cerebral ischemic attacks. However, it is crucial to be mindful that like other therapeutic armentarium, the efficacy of antioxidant gene transfer requires extensive preclinical investigation before it can be used in patients, and that it may have unanticipated short- or long-term adverse effects. Thus, it is critical to balance between the therapeutic benefits and potential risks, to develop disease-specific antioxidant gene transfer strategies, to deliver the therapy with an optimal time window and in a safe manner. This review attempts to provide the rationale, the most effective approaches and the potential hurdles of available antioxidant gene transfer approaches for ischemic injury in various organs, as well as the possible directions of future preclinical and clinical investigations of this highly promising therapeutic modality.

Indexed as

Gene Transfer TechniquesAnimalsAntioxidantsGenetic TherapyHumansIschemiaOxidative StressReactive Oxygen SpeciesAntioxidantsReactive Oxygen Species

Identifiers

PMID19233238
PMCPMC2691416
OpenAlexW1984006376

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.