Evidence map›Paper›PMID 35955530›Full record

ReviewInternational journal of molecular sciences2022

Molecular Mechanisms Underlying Intensive Care Unit-Acquired Weakness and Sarcopenia.

Marcela Kanova, Pavel Kohout

2 registry-linked trialsOpen access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.5field-weighted citation impact, top 4% 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.

NCT05991778 completednot on this map

Bioelectrical Impedance Vector Analysis (BIVA) in Monitoring Hyperhydration and Polyneuromyopathy in Critically Ill Patients

TypeobservationalSponsorUniversity Hospital OstravaRan2021 to 2022Enrolled61ConditionsRespiratory Distress Syndrome, Acute, Respiratory Insufficiency, Lung Ventilator, HyperhydrationArmsBioelectrical impedance vector analysis (BIVA), Blood and urine analysis, cumulative water balance
NCT07017517 narecruitingnot on this mapstarted 2026, after this paper: background citation

Effect of Physical Therapy on NLRP3 Inflammasome Activation and Muscle Atrophy in Critical Illness Myopathy (PT-NLRP3-CIM).

TypeinterventionalSponsorUniversity of ChileRan2026 to 2027Enrolled24ConditionsCritical Illness MyopathyArmsMotomed Letto® servo-assisted cycling + standard physiotherapy, Standard physiotherapy
3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Mitochondrial Quality Control and Cell Death.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Observational
  10. Observational
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Intensive care unit-acquired weakness: Recent insights.Journal of intensive medicine · 2024
    Review
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

2 authors at 2 institutions in 1 country.

Marcela KanovaDepartment of Anaesthesiology and Intensive Care Medicine, University Hospital Ostrava, 708 52 Ostrava, Czech Republic.ORCID 0000-0001-8880-8925
Pavel KohoutDepartment of Internal Medicine, 3rd Faculty of Medicine, Charles University Prague and Teaching Thomayer Hospital, 140 59 Prague, Czech Republic.ORCID 0000-0002-3957-7005
Charles University · CZUniversity of Ostrava · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle is a highly adaptable organ, and its amount declines under catabolic conditions such as critical illness. Aging is accompanied by a gradual loss of muscle, especially when physical activity decreases. Intensive care unit-acquired weakness is a common and highly serious neuromuscular complication in critically ill patients. It is a consequence of critical illness and is characterized by a systemic inflammatory response, leading to metabolic stress, that causes the development of multiple organ dysfunction. Muscle dysfunction is an important component of this syndrome, and the degree of catabolism corresponds to the severity of the condition. The population of critically ill is aging; thus, we face another negative effect-sarcopenia-the age-related decline of skeletal muscle mass and function. Low-grade inflammation gradually accumulates over time, inhibits proteosynthesis, worsens anabolic resistance, and increases insulin resistance. The cumulative consequence is a gradual decline in muscle recovery and muscle mass. The clinical manifestation for both of the above conditions is skeletal muscle weakness, with macromolecular damage, and a common mechanism-mitochondrial dysfunction. In this review, we compare the molecular mechanisms underlying the two types of muscle atrophy, and address questions regarding possible shared molecular mechanisms, and whether critical illness accelerates the aging process.

Indexed as

Muscular DiseasesSarcopeniaCritical IllnessHumansIntensive Care UnitsMuscle, SkeletalMuscle WeaknessMuscular Atrophyintensive care unit-acquired weaknessmuscle atrophyproteostasisrapamycin systemsarcopeniaubiquitin–proteasome system

Identifiers

PMID35955530
PMCPMC9368893
OpenAlexW4289134597

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.