ReviewMediators of inflammation2017
Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells?
Review in Mediators of inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.
What it found
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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.
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Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
- "Immunopause" no more: exercise to counter immunosenescence in aging.Immunity & ageing : I & A · 2025Review
- Review
- Recent advances and applications of mitochondria in tumors and inflammation.Journal of translational medicine · 2025Review
- Inflammatory Trajectory of Type 2 Diabetes: Novel Opportunities for Early and Late Treatment.Cells · 2024Review
- Mitochondrial microRNAs: New Emerging Players in Vascular Senescence and Atherosclerotic Cardiovascular Disease.International journal of molecular sciences · 2024Review
- The Molecular Mechanisms in Senescent Cells Induced by Natural Aging and Ionizing Radiation.Cells · 2024Review
- A pathological convergence theory for non-communicable diseases.Aging medicine (Milton (N.S.W)) · 2023Review
- Assessment of the expression of microRNAs‑221‑3p, ‑146a‑5p, ‑16‑5p and BCL2 in oncocytic carcinoma of the breast: A case report.Oncology letters · 2023Article
- Research progress and hot spot analysis related to oxidative stress and osteoarthritis: a bibliometric analysis.BMC musculoskeletal disorders · 2023Article
- Mitochondria Localized microRNAs: An Unexplored miRNA Niche in Alzheimer's Disease and Aging.Cells · 2023Review
- Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023Review
- Mitochondrial-related microRNAs and their roles in cellular senescence.Frontiers in physiology · 2023Review
- Inhibition of miR-146a-5p and miR-8114 in Insulin-Secreting Cells Contributes to the Protection of Melatonin against Stearic Acid-Induced Cellular Senescence by Targeting Mafa.Endocrinology and metabolism (Seoul, Korea) · 2022Article
- Repurposing SGLT-2 Inhibitors to Target Aging: Available Evidence and Molecular Mechanisms.International journal of molecular sciences · 2022Review
- MicroRNA expression profiles in extracellular vesicles and intracellular of AURKA inhibitor-induced senescent neuroblastoma cells.Translational cancer research · 2022Article
- Renal mitochondrial injury in the pathogenesis of CKD: mtDNA and mitomiRs.Clinical science (London, England : 1979) · 2022Review
- Effect of Hyperglycemia on COVID-19 Outcomes: Vaccination Efficacy, Disease Severity, and Molecular Mechanisms.Journal of clinical medicine · 2022Review
- Glutathione: A Samsonian life-sustaining small molecule that protects against oxidative stress, ageing and damaging inflammation.Frontiers in nutrition · 2022Review
- Review
- Review
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A relevant feature of aging is chronic low-grade inflammation, termed inflammaging, a key process promoting the development of all major age-related diseases. Senescent cells can acquire the senescence-associated (SA) secretory phenotype (SASP), characterized by the secretion of proinflammatory factors fuelling inflammaging. Cellular senescence is also accompanied by a deep reshaping of microRNA expression and by the modulation of mitochondria activity, both master regulators of the SASP. Here, we synthesize novel findings regarding the role of mitochondria in the SASP and in the inflammaging process and propose a network linking nuclear-encoded SA-miRNAs to mitochondrial gene regulation and function in aging cells. In this conceptual structure, SA-miRNAs can translocate to mitochondria (SA-mitomiRs) and may affect the energetic, oxidative, and inflammatory status of senescent cells. We discuss the potential role of several of SA-mitomiRs (i.e., let-7b, miR-1, miR-130a-3p, miR-133a, miR-146a-5p, miR-181c-5p, and miR-378-5p), using miR-146a as a proof-of-principle model. Finally, we propose a comprehensive, metabolic, and epigenetic view of the senescence process, in order to amplify the range of possible approaches to target inflammaging, with the ultimate goal of decelerating the aging rate, postponing or blunting the development of age-related diseases.
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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.