Evidence map›Paper›PMID 38934280›Full record

ReviewCurrent medicinal chemistry2025

Mitochondria and Lipid Droplets: Focus on the Molecular Structure of Contact Sites in the Pathogenesis of Metabolic Syndrome.

Larisa Sergeevna Litvinova, Maria Aleksandrovna Vulf, Kristina Alekseevna Yurova, Olga Gennadievna Khaziakhmatova, Vladimir Malashchenko, Maria Bograya, Ivan Kozlov, Natalia Todosenko

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current medicinal chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

8 authors.

Larisa Sergeevna LitvinovaCenter of Immunology and Cellular Biotechnology, Department of Basic Laboratory of Immunology and Cell Biotechnology, Immanuel Kant Baltic Federal University, Kaliningrad, Russia.ORCID 0000-0001-5231-6910
Maria Aleksandrovna VulfCenter of Immunology and Cellular Biotechnology, Department of Basic Laboratory of Immunology and Cell Biotechnology, Immanuel Kant Baltic Federal University, Kaliningrad, Russia.
Kristina Alekseevna YurovaCenter of Immunology and Cellular Biotechnology, Department of Basic Laboratory of Immunology and Cell Biotechnology, Immanuel Kant Baltic Federal University, Kaliningrad, Russia.ORCID 0000-0001-6146-3330
Olga Gennadievna KhaziakhmatovaCenter of Immunology and Cellular Biotechnology, Department of Basic Laboratory of Immunology and Cell Biotechnology, Immanuel Kant Baltic Federal University, Kaliningrad, Russia.ORCID 0000-0002-5525-3529
Vladimir MalashchenkoCenter of Immunology and Cellular Biotechnology, Department of Basic Laboratory of Immunology and Cell Biotechnology, Immanuel Kant Baltic Federal University, Kaliningrad, Russia.ORCID 0000-0003-3437-0926
Maria BograyaCenter of Immunology and Cellular Biotechnology, Department of Basic Laboratory of Immunology and Cell Biotechnology, Immanuel Kant Baltic Federal University, Kaliningrad, Russia.ORCID 0000-0002-4543-7850
Ivan KozlovInstitute of Professional Education, I.M. Sechenov First Moscow State Medical University, Moscow.
Natalia TodosenkoCenter of Immunology and Cellular Biotechnology, Department of Basic Laboratory of Immunology and Cell Biotechnology, Immanuel Kant Baltic Federal University, Kaliningrad, Russia.ORCID 0000-0001-7468-4861

Funding

Russian Science Foundation 23-15-00061
6 · The paper itself

Abstract

Metabolic syndrome (MetS) is a complex of serious pathologies with a high prevalence worldwide. Disruption of mitochondrial biogenesis and its interaction with other cell organelles plays an important role in the development of MetS. Studies have revealed the phenotypic and functional heterogeneity of mitochondria that exist within a single cell and can regulate metabolic signaling pathways, influencing the development of metabolic diseases. Excessive intake of fatty acids leads to changes in fatty acid metabolism that affect the biology of important cell organelles - the lipid droplets, whose specific biology is not fully understood. Perhaps targeted molecular genetic stimulation aimed at regulating the contact between mitochondria and lipids can break the vicious cycle of inflammation in MetS and restore normal cell function, reducing the risk of developing concomitant pathologies. The review describes potential (promising) therapeutic molecular targets associated with mitochondria and lipid droplets, focusing on the proteins involved in their contact and emphasizing their role in the pathogenesis of MetS.

Indexed as

Lipid DropletsMetabolic SyndromeMitochondriaAnimalsHumansMolecular Structurefattyinsulin resistancelipid dropletliver disease.Metabolic syndromemitochondria

Identifiers

PMID38934280

What OpenQuestion 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 OpenQuestion graph.