ArticlePloS one2016
Mitochondrial Haplogroups and Risk of Pulmonary Arterial Hypertension.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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.
Who cites it
19 citing papers in PubMed.
- Mitochondrial cardiovascular diseases: molecular mechanisms, multi-omics exploration and therapeutic strategies.Journal of advanced research · 2026Review
- Mitochondrial DNA haplogroups and circulating cell-free mitochondrial DNA as biomarkers of bronchopulmonary dysplasia.Pediatric research · 2025Article
- Mitochondrial genetics through the lens of single-cell multi-omics.Nature genetics · 2024Review
- Pulmonary Hypertension and Hyperglycemia-Not a Sweet Combination.Diagnostics (Basel, Switzerland) · 2024Review
- Extracellular vesicle mitochondrial DNA levels are associated with race and mitochondrial DNA haplogroup.iScience · 2024Article
- Recovery of mitogenomes from whole genome sequences to infer maternal diversity in 1883 modern taurine and indicine cattle.Scientific reports · 2022Article
- Epigenetic Mechanisms as Emerging Therapeutic Targets and Microfluidic Chips Application in Pulmonary Arterial Hypertension.Biomedicines · 2022Review
- Metabolism in Pulmonary Hypertension.Annual review of physiology · 2021Review
- 'There and Back Again'-Forward Genetics and Reverse Phenotyping in Pulmonary Arterial Hypertension.Genes · 2020Review
- Exploring New Therapeutic Pathways in Pulmonary Hypertension. Metabolism, Proliferation, and Personalized Medicine.American journal of respiratory cell and molecular biology · 2020Article
- Diagnosis and Management of Pulmonary Hypertension in the Modern Era: Insights from the 6th World Symposium.Pulmonary therapy · 2020Review
- Deconstructing the Melting Pot in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2020Article
- The role of genomics and genetics in pulmonary arterial hypertension.Global cardiology science & practice · 2020Review
- Mitochondrial DNA variation modulates alveolar development in newborn mice exposed to hyperoxia.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Genetics and genomics of pulmonary arterial hypertension.The European respiratory journal · 2019Review
- Mitochondrial dysfunction and pulmonary hypertension: cause, effect, or both.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- Mitochondrial DNA sequencing and large-scale genotyping identifiesOncotarget · 2017Article
- Pulmonary Hypertension and Precision Medicine through the "Omics" Looking Glass.American journal of respiratory and critical care medicine · 2017Article
- The Third Man: DNA sensing as espionage in pulmonary vascular health and disease.Pulmonary circulationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Pulmonary arterial hypertension (PAH) is a serious and often fatal disease. It is a panvasculopathy of the pulmonary microcirculation characterized by vasoconstriction and arterial obstruction due to vascular proliferation and remodeling and ultimately right ventricular failure. Mitochondrial dysfunction is a universal finding in pulmonary vascular cells of patients with PAH, and is mechanistically linked to disease origins in animal models of pulmonary hypertension. Mitochondria have their own circular DNA (mtDNA), which can be subgrouped into polymorphic haplogroup variants, some of which have been identified as at-risk or protective from cardiovascular and/or neurodegenerative diseases. Here, we hypothesized that mitochondrial haplogroups may be associated with PAH. To test this, mitochondrial haplogroups were determined in a cohort of PAH patients and controls [N = 204 Caucasians (125 PAH and 79 controls) and N = 46 African Americans (13 PAH and 33 controls)]. Haplogroup L was associated with a lower rate of PAH as compared to macrohaplogroups N and M. When haplogroups were nested based on ancestral inheritance and controlled for age, gender and race, haplogroups M and HV, JT and UK of the N macro-haplogroup had significantly higher rates of PAH compared to the ancestral L (L0/1/2 and L3) (all p ≤ 0.05). Overall, the findings suggest that mitochondrial haplogroups influence risk of PAH and that a vulnerability to PAH may have emerged under the selective enrichment of specific haplogroups that occurred with the migration of populations out of Africa.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.