Evidence map›Paper›PMID 29345195›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2018

Mitochondrial dysfunction and pulmonary hypertension: cause, effect, or both.

Jeffrey D Marshall, Isabel Bazan, Yi Zhang, Wassim H Fares, Patty J Lee

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Restoration of pp60International journal of molecular sciences · 2025
    Article
  13. Review
  14. Article
  15. Single-cell RNA sequencing: new insights for pulmonary endothelial cells.Frontiers in cell and developmental biology · 2025
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Mitochondria-derived Vesicle Packaging as a Novel Therapeutic Mechanism in Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2024
    Article

8 more citing papers are in PubMed but not listed here.

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 1 country.

Jeffrey D MarshallSection of Pulmonary, Critical Care, and Sleep Medicine, Yale University School of Medicine , New Haven, Connecticut.ORCID 0000-0002-1879-9274
Isabel BazanSection of Pulmonary, Critical Care, and Sleep Medicine, Yale University School of Medicine , New Haven, Connecticut.
Yi ZhangSection of Pulmonary, Critical Care, and Sleep Medicine, Yale University School of Medicine , New Haven, Connecticut.
Wassim H FaresSection of Pulmonary, Critical Care, and Sleep Medicine, Yale University School of Medicine , New Haven, Connecticut.
Patty J LeeSection of Pulmonary, Critical Care, and Sleep Medicine, Yale University School of Medicine , New Haven, Connecticut.
Yale University · US

Funding

Training Translational Lung Biology and PathobiologyT32HL007778 · NHLBI · YALE UNIVERSITY · PI Erica L Herzog, NAFTALI KAMINSKI · 1994 to 2026
$14.4M
TLR4-MEDIATED EPIGENETIC AND SENESCENCE MECHANISMS IN EMPHYSEMAR01HL138396 · NHLBI · YALE UNIVERSITY · PI LEE, PATTY J · 2017 to 2020
$1.5M
MIF-mediated Mechanisms in EmphysemaI01BX003265 · VA · VA CONNECTICUT HEALTHCARE SYSTEM · PI PATTY J LEE · 2017 to 2026
–
BLRD VA I01 BX003265NHLBI NIH HHS R01 HL138396NHLBI NIH HHS T32 HL007778
6 · The paper itself

Abstract

Pulmonary hypertension describes a heterogeneous disease defined by increased pulmonary artery pressures, and progressive increase in pulmonary vascular resistance due to pathologic remodeling of the pulmonary vasculature involving pulmonary endothelial cells, pericytes, and smooth muscle cells. This process occurs under various conditions, and although these populations vary, the clinical manifestations are the same: progressive dyspnea, increases in right ventricular (RV) afterload and dysfunction, RV-pulmonary artery uncoupling, and right-sided heart failure with systemic circulatory collapse. The overall estimated 5-yr survival rate is 72% in highly functioning patients, and as low as 28% for those presenting with advanced symptoms. Metabolic theories have been suggested as underlying the pathogenesis of pulmonary hypertension with growing evidence of the role of mitochondrial dysfunction involving the major proteins of the electron transport chain, redox-related enzymes, regulators of the proton gradient and calcium homeostasis, regulators of apoptosis, and mitophagy. There remain more studies needed to characterize mitochondrial dysfunction leading to impaired vascular relaxation, increase proliferation, and failure of regulatory mechanisms. The effects on endothelial cells and resulting interactions with their microenvironment remain uncharted territory for future discovery. Additionally, on the basis of observations that the "plexigenic lesions" of pulmonary hypertension resemble the unregulated proliferation of tumor cells, similarities between cancer pathobiology and pulmonary hypertension have been drawn, suggesting interactions between mitochondria and angiogenesis. Recently, mitochondria targeting has become feasible, which may yield new therapeutic strategies. We present a state-of-the-art review of the role of mitochondria in both the pathobiology of pulmonary hypertension and potential therapeutic targets in pulmonary vascular processes.

Indexed as

AnimalsHumansHypertension, PulmonaryMitochondriaMitochondrial Diseasesmitochondriapulmonary hypertension

Identifiers

PMID29345195
PMCPMC6008129
OpenAlexW2783340643

What Socratic 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 Socratic graph.