Evidence map›Paper›PMID 36235741›Full record

ReviewNutrients2022

Negative Effects of Chronic High Intake of Fructose on Lung Diseases.

Adrián Hernández-Díazcouder, Javier González-Ramírez, Fausto Sanchez, José J Leija-Martínez, Gustavo Martínez-Coronilla, Luis M Amezcua-Guerra, Fausto Sánchez-Muñoz

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 15% 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

6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Metformin attenuates fructose-induced pulmonary fibrosis, possibly through the involvement of the TRPC6 channel.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
    Article
  4. Article
  5. Review
  6. 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

7 authors at 4 institutions in 1 country.

Adrián Hernández-DíazcouderDepartment of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.ORCID 0000-0001-6569-2851
Javier González-RamírezCellular Biology Laboratory, Faculty of Nursing, Universidad Autónoma de Baja California Campus Mexicali, Mexicali 21100, Mexico.ORCID 0000-0002-7541-8773
Fausto SanchezDepartment of Agricultural and Animal Production, Universidad Autónoma Metropolitana Xochimilco, Mexico City 04960, Mexico.
José J Leija-MartínezMaster and Doctorate Program in Medical, Dental, and Health Sciences, Faculty of Medicine, Universidad Nacional Autónoma de México Campus Ciudad Universitaria, Mexico City 04510, Mexico.ORCID 0000-0002-7178-1786
Gustavo Martínez-CoronillaHistology Laboratory, Faculty of Medicine, Universidad Autónoma de Baja California Campus Mexicali, Mexicali 21100, Mexico.ORCID 0000-0003-2346-5508
Luis M Amezcua-GuerraDepartment of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.ORCID 0000-0002-6258-5732
Fausto Sánchez-MuñozDepartment of Immunology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City 14080, Mexico.ORCID 0000-0001-6556-1632
Instituto Nacional de Cardiología · MXUniversidad Autónoma de Baja California · MXHospital Infantil de México Federico Gómez · MXUniversidad Autónoma Metropolitana · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the modern diet, excessive fructose intake (>50 g/day) had been driven by the increase, in recent decades, of the consumption of sugar-sweetened beverages. This phenomenon has dramatically increased within the Caribbean and Latin American regions. Epidemiological studies show that chronic high intake of fructose related to sugar-sweetened beverages increases the risk of developing several non-communicable diseases, such as chronic obstructive pulmonary disease and asthma, and may also contribute to the exacerbation of lung diseases, such as COVID-19. Evidence supports several mechanisms—such as dysregulation of the renin−angiotensin system, increased uric acid production, induction of aldose reductase activity, production of advanced glycation end-products, and activation of the mTORC1 pathway—that can be implicated in lung damage. This review addresses how these pathophysiologic and molecular mechanisms may explain the lung damage resulting from high intake of fructose.

Indexed as

FructoseLung DiseasesAldehyde ReductaseHumansMechanistic Target of Rapamycin Complex 1Sweetening AgentsUric AcidAldehyde ReductaseFructoseMechanistic Target of Rapamycin Complex 1Sweetening AgentsUric Acidasthmachronic obstructive pulmonary diseasefructoselung diseasessugar-sweetened beverages

Identifiers

PMID36235741
PMCPMC9571075
OpenAlexW4303962246

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.