Evidence map›Paper›PMID 37777764›Full record

ReviewCellular & molecular biology letters2023

Oxidative stress as a key modulator of cell fate decision in osteoarthritis and osteoporosis: a narrative review.

Jana Riegger, Astrid Schoppa, Leonie Ruths, Melanie Haffner-Luntzer, Anita Ignatius

Open access · goldAbstract readReview
In one paragraph

Review in Cellular & molecular biology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed, 4 pooled it
44.3field-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

139 citing papers in PubMed, 4 syntheses or guidelines pooled it, 178 citations in OpenAlex.

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  12. Bone organoids and mitochondrial reprogramming.Journal of orthopaedic translation · 2026
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79 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

5 authors at 1 institution in 1 country.

Jana RieggerDivision for Biochemistry of Joint and Connective Tissue Diseases, Department of Orthopedics, Ulm University Medical Center, 89081, Ulm, Germany. jana.riegger@uni-ulm.de.ORCID http://orcid.org/0000-0003-0048-5047
Astrid SchoppaInstitute of Orthopedic Research and Biomechanics, Ulm University Medical Center, 89081, Ulm, Germany.
Leonie RuthsDivision for Biochemistry of Joint and Connective Tissue Diseases, Department of Orthopedics, Ulm University Medical Center, 89081, Ulm, Germany.
Melanie Haffner-LuntzerInstitute of Orthopedic Research and Biomechanics, Ulm University Medical Center, 89081, Ulm, Germany.
Anita IgnatiusInstitute of Orthopedic Research and Biomechanics, Ulm University Medical Center, 89081, Ulm, Germany.
Universität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During aging and after traumatic injuries, cartilage and bone cells are exposed to various pathophysiologic mediators, including reactive oxygen species (ROS), damage-associated molecular patterns, and proinflammatory cytokines. This detrimental environment triggers cellular stress and subsequent dysfunction, which not only contributes to the development of associated diseases, that is, osteoporosis and osteoarthritis, but also impairs regenerative processes. To counter ROS-mediated stress and reduce the overall tissue damage, cells possess diverse defense mechanisms. However, cellular antioxidative capacities are limited and thus ROS accumulation can lead to aberrant cell fate decisions, which have adverse effects on cartilage and bone homeostasis. In this narrative review, we address oxidative stress as a major driver of pathophysiologic processes in cartilage and bone, including senescence, misdirected differentiation, cell death, mitochondrial dysfunction, and impaired mitophagy by illustrating the consequences on tissue homeostasis and regeneration. Moreover, we elaborate cellular defense mechanisms, with a particular focus on oxidative stress response and mitophagy, and briefly discuss respective therapeutic strategies to improve cell and tissue protection.

Indexed as

OsteoarthritisOsteoporosisCell DifferentiationCellular SenescenceHumansOxidative StressReactive Oxygen SpeciesReactive Oxygen SpeciesBoneCartilageCell deathCell fate decisionMitochondrial dysfunctionOsteoarthritisOsteoporosisOxidative stressROSSenescence

Identifiers

PMID37777764
PMCPMC10541721
OpenAlexW4387209567

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.