Evidence map›Paper›PMID 33293849›Full record

ReviewJournal of inflammation research2020

Reactive Oxygen Species: Drivers of Physiological and Pathological Processes.

Javier Checa, Josep M Aran

Open access · goldAbstract readReview
In one paragraph

Review in Journal of inflammation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 495 papers.

0numbers the graph read from it
0cells of the map it votes in
495citing papers in PubMed
25.6field-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

495 citing papers in PubMed, 875 citations in OpenAlex.

  1. Article
  2. Impact of renal iron overload on sickle cell nephropathy in a humanized mouse model.American journal of physiology. Renal physiology · 2026
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  12. ZnbioRxiv : the preprint server for biology · 2026
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435 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

2 authors at 1 institution in 1 country.

Javier ChecaImmune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L'Hospitalet de Llobregat, Barcelona 08907, Spain.
Josep M AranImmune-Inflammatory Processes and Gene Therapeutics Group, IDIBELL, Hospital Duran i Reynals, L'Hospitalet de Llobregat, Barcelona 08907, Spain.
Duran i Reynals Hospital · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the Great Oxidation Event, about 2.4 billion years ago, the Earth is immersed in an oxidizing atmosphere. Thus, it has been proposed that excess oxygen, originally a waste product of photosynthetic cyanobacteria, induced oxidative stress and the production of reactive oxygen species (ROS), which have since acted as fundamental drivers of biologic evolution and eukaryogenesis. Indeed, throughout an organism's lifespan, ROS affect directly (as mutagens) or indirectly (as messengers and regulators) all structural and functional components of cells, and many aspects of cell biology. Whether left unchecked by protective antioxidant systems, excess ROS not only cause genomic mutations but also induce irreversible oxidative modification of proteins (protein oxidation and peroxidation), lipids and glycans (advanced lipoxidation and glycation end products), impairing their function and promoting disease or cell death. Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFκB/IκB, Nrf2/KEAP1, AP-1, p53, HIF-1). Consequently, ROS can shape a variety of cellular functions, including proliferation, differentiation, migration and apoptosis. In this review, we will give a brief overview of the relevance of ROS in both physiological and pathological processes, particularly inflammation and aging. In-depth knowledge of the molecular mechanisms of ROS actuation and their influence under steady-state and stressful conditions will pave the way for the development of novel therapeutic interventions. This will mitigate the harmful outcomes of ROS in the onset and progression of a variety of chronic inflammatory and age-related diseases.

Indexed as

inflammationoxidative stressreactive oxygen species

Identifiers

PMID33293849
PMCPMC7719303
OpenAlexW3108095894

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.