Evidence map›Paper›PMID 26906267›Full record

ReviewAntioxidants & redox signaling2016

Oxidant Mechanisms in Renal Injury and Disease.

Brian B Ratliff, Wasan Abdulmahdi, Rahul Pawar, Michael S Wolin

Open access · hybridAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 349 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
349citing papers in PubMed, 1 pooled it
29.1field-weighted citation impact, top 1% 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

349 citing papers in PubMed, 1 synthesis or guideline pooled it, 677 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Assessment of ion release, cytotoxicity, and potential systemic toxicity of titanium dental alloy.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Article
  5. CMolecules (Basel, Switzerland) · 2026
    Article
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289 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Brian B Ratliff1 Department of Medicine, Renal Research Institute , New York Medical College, Valhalla, New York.
Wasan Abdulmahdi2 Department of Physiology, Renal Research Institute , New York Medical College, Valhalla, New York.
Rahul Pawar1 Department of Medicine, Renal Research Institute , New York Medical College, Valhalla, New York.
Michael S Wolin2 Department of Physiology, Renal Research Institute , New York Medical College, Valhalla, New York.
New York Medical College · US

Funding

Ferrochelatase & guanylate cyclase regulation in vascular dysfunctionR01HL129797 · NHLBI · NEW YORK MEDICAL COLLEGE · PI SUN, DONG, WOLIN, MICHAEL S · 2016 to 2019
$1.6M
ecSOD derived peroxide in pulmonary adaptation to hypoxiaR01HL115124 · NHLBI · NEW YORK MEDICAL COLLEGE · PI WOLIN, MICHAEL S · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL115124NHLBI NIH HHS R01 HL129797
6 · The paper itself

Abstract

significanceA common link between all forms of acute and chronic kidney injuries, regardless of species, is enhanced generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) during injury/disease progression. While low levels of ROS and RNS are required for prosurvival signaling, cell proliferation and growth, and vasoreactivity regulation, an imbalance of ROS and RNS generation and elimination leads to inflammation, cell death, tissue damage, and disease/injury progression. RECENT ADVANCES: Many aspects of renal oxidative stress still require investigation, including clarification of the mechanisms which prompt ROS/RNS generation and subsequent renal damage. However, we currently have a basic understanding of the major features of oxidative stress pathology and its link to kidney injury/disease, which this review summarizes. CRITICAL ISSUES: The review summarizes the critical sources of oxidative stress in the kidney during injury/disease, including generation of ROS and RNS from mitochondria, NADPH oxidase, and inducible nitric oxide synthase. The review next summarizes the renal antioxidant systems that protect against oxidative stress, including superoxide dismutase and catalase, the glutathione and thioredoxin systems, and others. Next, we describe how oxidative stress affects kidney function and promotes damage in every nephron segment, including the renal vessels, glomeruli, and tubules. FUTURE DIRECTIONS: Despite the limited success associated with the application of antioxidants for treatment of kidney injury/disease thus far, preventing the generation and accumulation of ROS and RNS provides an ideal target for potential therapeutic treatments. The review discusses the shortcomings of antioxidant treatments previously used and the potential promise of new ones. Antioxid. Redox Signal. 25, 119-146.

Indexed as

Disease SusceptibilityOxidative StressAnimalsAntioxidantsHumansKidneyKidney DiseasesKidney GlomerulusKidney TubulesLeukocytesMitochondriaOxidantsOxidation-ReductionReactive Oxygen SpeciesRenal CirculationAntioxidantsOxidantsReactive Oxygen Species

Identifiers

PMID26906267
PMCPMC4948213
OpenAlexW2346697308

What OpenQuestion holds

Textmetadata
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.