Evidence map›Paper›PMID 31853040›Full record

ReviewHypertension research : official journal of the Japanese Society of Hypertension2020

Role of complement 3 in the pathogenesis of hypertension.

Lan Chen, Noboru Fukuda, Taro Matsumoto, Masanori Abe

Abstract readReview
PubMed Publisher
In one paragraph

Review in Hypertension research : official journal of the Japanese Society of Hypertension, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  11. TWIST1 transcriptionally upregulates complement 3 in glomerular mesangial cells from spontaneously hypertensive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Article
  12. Review
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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.

Lan ChenDivision of Nephrology, Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, 173-8610, Japan.
Noboru FukudaDivision of Nephrology, Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, 173-8610, Japan. fukuda.noboru@nihon-u.ac.jp.
Taro MatsumotoDivision of Cell Regeneration and Transplantation, Department of Functional Morphology, Nihon University School of Medicine, Tokyo, 173-8610, Japan.
Masanori AbeDivision of Nephrology, Hypertension and Endocrinology, Department of Medicine, Nihon University School of Medicine, Tokyo, 173-8610, Japan. abe.masanori@nihon-u.ac.jp.
Nihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system has recently been reported to contribute to the development and pathogenesis of hypertension, several cardiovascular and renal diseases, and cardiometabolic disorders accompanied by inflammation and tissue remodeling. We have demonstrated that complement 3 (C3) is highly expressed in mesenchymal tissues in spontaneously hypertensive rats (SHRs) and induces the synthetic phenotype and exaggerated growth of mesenchymal cells by maintenance effect on dedifferentiated cells. To verify the role of C3 in the pathogenesis of hypertension, we targeted the C3 gene from SHRs by zinc-finger nuclease gene-editing technology and demonstrated that the increased expression of C3 induces salt-sensitive hypertension with activation of the renal renin-angiotensin system in SHRs. We recently found that increased expression of C3 is associated with the suppression of miR145 and induces Krüppel-like factor 5 and the synthetic phenotype of mesenchymal cells in SHRs. We also demonstrated that C3 is involved in the epithelial-to-mesenchymal transition and dedifferentiation of epithelial cells in kidneys subjected to unilateral ureteral obstruction with elevation of blood pressure. Thus, C3 is an essential factor in the pathogenesis of hypertension due to its maintenance effect on undifferentiated mesenchymal cells.

Indexed as

AnimalsComplement C3Epithelial-Mesenchymal TransitionHumansHypertensionKidneyRatsRats, Inbred SHRRenin-Angiotensin SystemComplement C3Complement 3Epithelial-to-mesenchymal transitionHypertension Mesenchymal cellSpontaneously hypertensive rat

Identifiers

PMID31853040
OpenAlexW2994963717

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.