Evidence map›Paper›PMID 35172853›Full record

ArticleOrphanet journal of rare diseases2022

Assessing the role of blood pressure in amyotrophic lateral sclerosis: a Mendelian randomization study.

Kailin Xia, Linjing Zhang, Lu Tang, Tao Huang, Dongsheng Fan

Open access · goldAbstract read
In one paragraph

Article in Orphanet journal of rare diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Causal role of MiRNAs in chronic rhinosinusitis: mendelian randomization and validation study.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2025
    Article
  5. Role of lipocalin-2 in amyotrophic lateral sclerosis.Frontiers in aging neuroscience · 2025
    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

5 authors at 1 institution in 2 countries.

Kailin XiaDepartment of Neurology, Peking University Third Hospital, Garden North Road No. 49, Beijing, 100191, China.
Linjing ZhangDepartment of Neurology, Peking University Third Hospital, Garden North Road No. 49, Beijing, 100191, China.
Lu TangDepartment of Neurology, Peking University Third Hospital, Garden North Road No. 49, Beijing, 100191, China.
Tao Huang *Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China. huangtao@bjmu.edu.cn.
Dongsheng Fan *Department of Neurology, Peking University Third Hospital, Garden North Road No. 49, Beijing, 100191, China. dsfan2010@aliyun.com.ORCID 0000-0002-3129-9821
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObservational studies have suggested a close but controversial relationship between blood pressure (BP) and amyotrophic lateral sclerosis (ALS). It remains unclear whether this association is causal. The authors employed a bidirectional two-sample Mendelian randomization (MR) approach to evaluate the causal relationship between BP and ALS. Genetic proxies for systolic blood pressure (SBP), diastolic blood pressure (DBP), antihypertensive drugs (AHDs), ALS, and their corresponding genome-wide association study (GWAS) summary datasets were obtained from the most recent studies with the largest sample sizes. The inverse variance weighted (IVW) method was adopted as the main approach to examine the effect of BP on ALS and four other MR methods were used for sensitivity analyses. To exclude the interference between SBP and DBP, a multivariable MR approach was used.

resultsWe found that genetically determined increased DBP was a protective factor for ALS (OR = 0.978, 95% CI 0.960-0.996, P = 0.017) and that increased SBP was an independent risk factor for ALS (OR = 1.014, 95% CI 1.003-1.025, P = 0.015), which is supported by sensitivity analyses. The use of calcium channel blocker (CCB) showed a causal relationship with ALS (OR = 0.985, 95% CI 0.971-1.000, P = 0.049). No evidence was revealed that ALS caused changes in BP.

conclusionsThis study provides genetic support for a causal effect of BP and ALS that increased DBP has a protective effect on ALS, and increased SBP is a risk factor for ALS, which may be related to sympathetic excitability. Blood pressure management is essential in ALS, and CCB may be a promising candidate.

Indexed as

Amyotrophic Lateral SclerosisBlood PressureGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideRisk FactorsAmyotrophic lateral sclerosisBlood pressureCalcium channel blockerMendelian randomization

Identifiers

PMID35172853
PMCPMC8848798
OpenAlexW4220882153

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.