Evidence mapPaperPMID 42212385Full record

ReviewClinical science (London, England : 1979)2026

Sex-dependent differences in mitochondrial protein acetylation in metabolic condition, oxidative stress, vascular dysfunction, hypertension, and cardiovascular disease.

Anna Dikalova, Sergey Dikalov

Abstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Anna DikalovaVanderbilt University Medical Center, Nashville, Tennessee, U.S.A.
Sergey DikalovVanderbilt University Medical Center, Nashville, Tennessee, U.S.A.ORCID 0000-0003-2976-6184

Funding

American Heart Association (AHA) 19TPA34910157American Heart Association (AHA) 23TPA1077648HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL183432HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) RO1HL144943HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) RO1HL157583
6 · The paper itself

Abstract

One half of adults have hypertension, which is a major risk factor for stroke, myocardial infarction, heart failure, and vascular dementia. There is an urgent need for new therapies, particularly for women with hypertension. Hypertension affects women in all phases of life; however, the hypertension rate increases in women much more steeply, and hypertensive vascular and kidney damage is significantly higher in women. Despite great burden, only 1 in 4 patients have their blood pressure under control. Hypertension accounts for 1 in 5 deaths among American women, posing a greater burden for women than men. Meanwhile, female-specific aspects of hypertension are poorly understood, and women or female-specific risk factors are understudied in basic, clinical, and population research and hypertension guidelines. Understanding these mechanisms can help to develop new therapies. Endothelial dysfunction has a profound prognostic implication predicting adverse cardiovascular events. We suggest that female antihypertensive protection is critically dependent on mitochondrial pathways preserving endothelial function. Metabolic disorders and oxidative stress contribute to the pathogenesis of these conditions, which are linked to mitochondrial dysfunction. Proteomic studies showed higher expression of mitochondrial fatty acid oxidation and antioxidant enzymes in females, and oxidative damage is lower in females compared with males. Meanwhile, the actual activity of these mitochondrial metabolic and antioxidant enzymes is regulated by acetylation, but sex-specific differences in mitochondrial acetylation in vascular disease have not been studied. In the present review, we will discuss potential sex differences in mitochondrial protein acetylation and its implications in metabolic conditions, oxidative stress, vascular dysfunction, hypertension, and cardiovascular disease.

Indexed as

Cardiovascular DiseasesHypertensionMitochondriaMitochondrial ProteinsOxidative StressAcetylationAnimalsFemaleHumansMaleRisk FactorsSex CharacteristicsSex FactorsMitochondrial Proteinsacetylationantioxidanthypertensionmitochondriaoxidative stresssex

Identifiers

PMID42212385
PMCPMC13223376

What Socratic holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.