ReviewMolecular biology reports2022
Inflammatory-associated apoptotic markers: are they the culprit to rheumatoid arthritis pain?
Review in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Programmed Cell Death in Rheumatoid Arthritis.Journal of inflammation research · 2025Review
- Novel insights into the crosstalk between non-coding RNA and apoptosis in rheumatoid arthritis: diagnostic functions and therapeutic applications.Frontiers in immunology · 2025Review
- Depressive symptoms and all-cause mortality among middle-aged and older people in China and associations with chronic diseases.Frontiers in public health · 2024Article
- Morphological and Mechanical Characterization of Extracellular Vesicles and Parent Human Synoviocytes under Physiological and Inflammatory Conditions.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundRheumatoid arthritis (RA) is a prolonged inflammatory disease resulting from autoimmune reactions that leads to local and systemic bone erosion, joint defects and functional impairment. Although the inflammation is subsided through the prescription of anti-inflammatory therapeutics, the patients persistently complained of sleepless nights due to flare pain. This indicates the possible contribution of other pathways besides inflammation in leading to RA pain. This review aims to uncover the roles and involvement of several inflammatory-associated apoptotic markers in facilitating pain transmission and processing during the pathogenesis of RA. MATERIALS AND
methodsThis narrative review focused on the reports from the previous literature based on the search string of "apoptotic marker AND inflammation AND 'chronic pain' OR 'neuropathic pain' and apoptosis AND 'rheumatoid arthritis' OR arthritis from the databases including Science Direct and Scopus, considering the exclusion criteria of the published abstracts, proceedings or articles on other neuropathic pain types such as painful bowel syndrom, insterstitial cystitis, fibrosis and so on.
resultsSeveral studies in the literature demonstrate a close association between imbalanced apoptotic regulations and an increased number of synovial fibroblasts and inflammatory cells in RA. Cell death or specific cell survival has been linked with increased central hypersensitivity in various types of chronic and neuropathic pain.
conclusionThe RA-related flare pain is possibly contributed by the abnormal regulation of apoptosis through several inflammatory-related pathways, and further studies need to modulate these pathways for the putative anti-nociceptive benefits.
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What OpenQuestion holds
Registered trials
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.