ArticleScientific reports2016
Macrophage Migration Inhibitory Factor (MIF) Deficiency Exacerbates Aging-Induced Cardiac Remodeling and Dysfunction Despite Improved Inflammation: Role of Autophagy Regulation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 69 citations in OpenAlex.
- Article
- Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies.Biomolecules · 2026Review
- Modeling Fungal and Amoebic Infections: Co-culture Approaches to Study MIF's Role in Infection-Induced Inflammatory Responses.Methods in molecular biology (Clifton, N.J.) · 2026Article
- MIF Regulates the Th17/Treg Ratio to Exacerbate Kidney Injury in Chronic Kidney Disease.Inflammation · 2025Article
- The multifaced role of the macrophage migration inhibitory factor family in organ fibrosis.American journal of physiology. Cell physiology · 2025Review
- Cancer therapy-related cardiovascular aging: mechanisms, monitoring, and intervention strategies.Frontiers in cardiovascular medicine · 2025Review
- The dichotomic role of cytokines in aging.Biogerontology · 2024Review
- MIF Inhibition by ISO-1 Decreased Autophagic Activity in Primary Astrocytes During Cobalt Chloride-Induced Hypoxia.Current issues in molecular biology · 2024Article
- Inflammation in atherosclerosis: pathophysiology and mechanisms.Cell death & disease · 2024Review
- Overexpression of macrophage migration inhibitory factor protects against pressure overload-induced cardiac hypertrophy through regulating the miR-29b-3p/HBP1 axis.Physiological reports · 2024Article
- Macrophage migration inhibitory factor reversed senescent phenotype in human chondrocytes in vitro.Molecular biology reports · 2024Article
- Systemic immune profile in Prader-Willi syndrome: elevated matrix metalloproteinase and myeloperoxidase and reduced macrophage inhibitory factor.Orphanet journal of rare diseases · 2023Article
- Circulating biomarkers for management of cancer therapeutics-related cardiac dysfunction.Cardiovascular research · 2023Review
- The Innate Immune System in Cardiovascular Diseases and Its Role in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2022Review
- Modern Concepts in Cardiovascular Disease: Inflamm-Aging.Frontiers in cell and developmental biology · 2022Review
- Regulated cell death pathways in doxorubicin-induced cardiotoxicity.Cell death & disease · 2021Review
- Autocrine Signaling in Cardiac Remodeling: A Rich Source of Therapeutic Targets.Journal of the American Heart Association · 2021Review
- Deficiency of MIF Accentuates Overloaded Compression-Induced Nucleus Pulposus Cell Oxidative Damage via Depressing Mitophagy.Oxidative medicine and cellular longevity · 2021Article
- Metabolic Complications in Cardiac Aging.Frontiers in physiology · 2021Review
- The Role of Macrophage Migration Inhibitory Factor (MIF) in Asthmatic Airway Remodeling.Allergy, asthma & immunology research · 2021Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Aging leads to unfavorable geometric and functional sequelae in the heart. The proinflammatory cytokine macrophage migration inhibitory factor (MIF) plays a role in the maintenance of cardiac homeostasis under stress conditions although its impact in cardiac aging remains elusive. This study was designed to evaluate the role of MIF in aging-induced cardiac anomalies and the underlying mechanism involved. Cardiac geometry, contractile and intracellular Ca(2+) properties were examined in young (3-4 mo) or old (24 mo) wild type and MIF knockout (MIF(-/-)) mice. Our data revealed that MIF knockout exacerbated aging-induced unfavorable structural and functional changes in the heart. The detrimental effect of MIF knockout was associated with accentuated loss in cardiac autophagy with aging. Aging promoted cardiac inflammation, the effect was attenuated by MIF knockout. Intriguingly, aging-induced unfavorable responses were reversed by treatment with the autophagy inducer rapamycin, with improved myocardial ATP availability in aged WT and MIF(-/-) mice. Using an in vitro model of senescence, MIF knockdown exacerbated doxorubicin-induced premature senescence in H9C2 myoblasts, the effect was ablated by MIF replenishment. Our data indicated that MIF knockout exacerbates aging-induced cardiac remodeling and functional anomalies despite improved inflammation, probably through attenuating loss of autophagy and ATP availability in the heart.
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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.