Evidence map›Paper›PMID 23894370›Full record

ArticlePloS one2013

Interleukin-16 promotes cardiac fibrosis and myocardial stiffening in heart failure with preserved ejection fraction.

Shunsuke Tamaki, Toshiaki Mano, Yasushi Sakata, Tomohito Ohtani, Yasuharu Takeda, Daisuke Kamimura, Yosuke Omori, Yasumasa Tsukamoto, Yukitoshi Ikeya, Mari Kawai and 9 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.5field-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

49 citing papers in PubMed, 93 citations in OpenAlex.

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  9. Role of epicardial adipose tissue in heart failure with preserved ejection fraction: An emerging molecular mechanism and therapeutic potential.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
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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

19 authors at 4 institutions in 1 country.

Shunsuke TamakiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Japan.
Toshiaki Mano
Yasushi Sakata
Tomohito Ohtani
Yasuharu Takeda
Daisuke Kamimura
Yosuke Omori
Yasumasa Tsukamoto
Yukitoshi Ikeya
Mari Kawai
Atsushi Kumanogoh
Keisuke Hagihara
Ryohei Ishii
Mitsuru Higashimori
Makoto Kaneko
Hidetoshi Hasuwa
Takeshi Miwa
Kazuhiro Yamamoto
Issei Komuro
Osaka University · JPNihon University · JPTottori University · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic heart failure (CHF) with preserved left ventricular (LV) ejection fraction (HFpEF) is observed in half of all patients with CHF and carries the same poor prognosis as CHF with reduced LV ejection fraction (HFrEF). In contrast to HFrEF, there is no established therapy for HFpEF. Chronic inflammation contributes to cardiac fibrosis, a crucial factor in HFpEF; however, inflammatory mechanisms and mediators involved in the development of HFpEF remain unclear. Therefore, we sought to identify novel inflammatory mediators involved in this process. METHODS AND

resultsAn analysis by multiplex-bead array assay revealed that serum interleukin-16 (IL-16) levels were specifically elevated in patients with HFpEF compared with HFrEF and controls. This was confirmed by enzyme-linked immunosorbent assay in HFpEF patients and controls, and serum IL-16 levels showed a significant association with indices of LV diastolic dysfunction. Serum IL-16 levels were also elevated in a rat model of HFpEF and positively correlated with LV end-diastolic pressure, lung weight and LV myocardial stiffness constant. The cardiac expression of IL-16 was upregulated in the HFpEF rat model. Enhanced cardiac expression of IL-16 in transgenic mice induced cardiac fibrosis and LV myocardial stiffening accompanied by increased macrophage infiltration. Treatment with anti-IL-16 neutralizing antibody ameliorated cardiac fibrosis in the mouse model of angiotensin II-induced hypertension.

conclusionOur data indicate that IL-16 is a mediator of LV myocardial fibrosis and stiffening in HFpEF, and that the blockade of IL-16 could be a possible therapeutic option for HFpEF.

Indexed as

Stroke VolumeAgedAged, 80 and overAnimalsDisease Models, AnimalFemaleFibrosisHeart FailureHemodynamicsHumansHypertensionInterleukin-16MacrophagesMaleMiceMice, TransgenicInterleukin-16

Identifiers

PMID23894370
PMCPMC3716890
OpenAlexW2084341751

What OpenQuestion holds

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Registered trials

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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.