Evidence map›Paper›PMID 35364736›Full record

ReviewInflammopharmacology2022

Elucidating the role of hypoxia-inducible factor in rheumatoid arthritis.

Essa M Sabi, Anuja Singh, Ziyad M Althafar, Tapan Behl, Aayush Sehgal, Sukhbir Singh, Neelam Sharma, Saurabh Bhatia, Ahmed Al-Harrasi, Hosam M Alqahtani and 1 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  17. Receptors expressions on peripheral lymphocytes and CD4Immunity, inflammation and disease · 2023
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  20. Arthritic Microenvironment Actuated Nanomotors for Active Rheumatoid Arthritis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
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

11 authors at 5 institutions in 4 countries.

Essa M SabiDepartment of Pathology, Clinical Biochemistry Unit, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Anuja SinghChitkara College of Pharmacy, Chitkara University, Patiala, Punjab, India.
Ziyad M AlthafarDepartment of Medical Laboratories Sciences, College of Applied Medical Sciences in Alquwayiyah, Shaqra University, Riyad, Saudi Arabia.
Tapan BehlChitkara College of Pharmacy, Chitkara University, Patiala, Punjab, India. tapanbehl31@gmail.com.ORCID http://orcid.org/0000-0003-0993-7708
Aayush SehgalChitkara College of Pharmacy, Chitkara University, Patiala, Punjab, India.
Sukhbir SinghChitkara College of Pharmacy, Chitkara University, Patiala, Punjab, India.
Neelam SharmaChitkara College of Pharmacy, Chitkara University, Patiala, Punjab, India.
Saurabh BhatiaNatural & Medical Sciences Research Centre, University of Nizwa, Nizwa, Oman.
Ahmed Al-HarrasiNatural & Medical Sciences Research Centre, University of Nizwa, Nizwa, Oman.
Hosam M AlqahtaniGeneral Directorate of Medical Service, Ministry of Interior, Riyadh, Kingdom of Saudi Arabia.
Simona BungauDepartment of Pharmacy, Faculty of Medicine and Pharmacy, University of Oradea, Oradea, Romania.
Chitkara University · INUniversity of Nizwa · OMKing Saud University · SAShaqra University · SAUniversity of Oradea · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a chronic multifactorial disease, provocative, and degenerative autoimmune condition that impacts millions of individuals around the globe. As a result of this understanding, anti-inflammatory drugs have been created, perhaps widely effective (like steroids) and highly specialized methods (including anti-TNF antibody) using biological therapies (including TNF inhibitors). Despite this, the connections between inflammatory response, articular development, and intracellular responsiveness to changes in oxygen concentration are undervalued in rheumatoid arthritis. Hypoxia, or a lack of oxygen, is thought to cause enhanced synovial angiogenesis in RA, which is mediated by some of the hypoxia-inducible factors like vascular endothelial growth factor (VEGF). Substantial genetic alterations occur when the HIF regulatory factors signaling cycle is activated, allowing organelles, tissues, and species to acclimatize to decreasing oxygen saturation. The most well-characterized hypoxia-responsive transcripts are the angiogenic stimulant VEGF, whose production is greatly elevated by hypoxia in several types of cells, especially RA synovium fibroblasts. Blocking vascular endothelial growth factors has been demonstrated to be helpful in murine models of rheumatism, indicating how hypoxia could trigger the angiogenesis process, resulting in the progression of RA. These mechanisms highlight the intimate affiliation amongst hypoxia, angiogenesis, and inflammation in rheumatoid arthritis. This review will look at how hypoxia activates molecular pathways and how other pathways involving inflammatory signals develop and sustain synovitis in rheumatoid arthritis.

Indexed as

Arthritis, RheumatoidVascular Endothelial Growth Factor AAnimalsHumansHypoxiaMiceNeovascularization, PathologicOxygenTumor Necrosis Factor InhibitorsOxygenTumor Necrosis Factor InhibitorsVascular Endothelial Growth Factor AAngiogenesisHypoxia-inducible factorInflammationRegulationRheumatoid arthritis

Identifiers

PMID35364736
OpenAlexW4226006759

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.