Interleukin‐6 neutralization ameliorates symptoms in prematurely aged mice
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Hutchinson–Gilford progeria syndrome (HGPS) causes premature aging in children, with adipose tissue, skin and bone deterioration, and cardiovascular impairment. In HGPS cells and mouse models, high levels of interleukin‐6, an inflammatory cytokine linked to aging processes, have been detected. Here, we show that inhibition of interleukin‐6 activity by tocilizumab, a neutralizing antibody raised against interleukin‐6 receptors, counteracts progeroid features in both HGPS fibroblasts and Lmna G609G / G609G progeroid mice. Tocilizumab treatment limits the accumulation of progerin, the toxic protein produced in HGPS cells, rescues nuclear envelope and chromatin abnormalities, and attenuates the hyperactivated DNA damage response. In vivo administration of tocilizumab reduces aortic lesions and adipose tissue dystrophy, delays the onset of lipodystrophy and kyphosis, avoids motor impairment, and preserves a good quality of life in progeroid mice. This work identifies tocilizumab as a valuable tool in HGPS therapy and, speculatively, in the treatment of a variety of aging‐related disorders.
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The LmnaG609G mouse model closely resembles human phenotypes, including heightened inflammation markers like IL-6, caspase 1, and Nlrp3, increased oxidative stress, persistent DNA damage, and cell cycle arrest.
“Among these models, the LmnaG609G mouse model (featuring the mutation 1827C > T; Gly609Gly) closely resembles human phenotypes.305 This includes heightened inflammation markers like IL-6, caspase 1, and Nlrp3, increased oxidative stress, persistent DNA damage, and cell cycle arrest.306,307”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [306]
Citation 305 is attached to the first sentence, not the subsequent list of inflammation and damage markers, which cites 306 and 307. The Materials and Methods (Mice; page unavailable) identifies the Lmna G609G mouse mutation as equivalent to the human HGPS LMNA G608G mutation, and the Results describe HGPS-related disease features in the mice. Our copy does not specify the claimed 1827C>T nucleotide change. (LLM, conf=0.82)
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“This includes heightened inflammation markers like IL-6, caspase 1, and Nlrp3, increased oxidative stress, persistent DNA damage, and cell cycle arrest.(306,307) In addition, two independently generated mouse models deficient in the Zmpste24 gene (Zmpste24− /− mice) also exhibit elevated expression of caspase 1 and Nl…”
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Mitophagy defect mediates the aging‐associated hallmarks in Hutchinson–Gilford progeria syndrome
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Inflammation and Fibrosis in Progeria: Organ-Specific Responses in an HGPS Mouse Model
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At the nucleus of cancer: how the nuclear envelope controls tumor progression
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Progerin, an Aberrant Spliced Form of Lamin A, Is a Potential Therapeutic Target for HGPS
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Non-Genomic Hallmarks of Aging—The Review
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The NLRP3 inhibitor Dapansutrile improves the therapeutic action of lonafarnib on progeroid mice
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Skeletal phenotypes and molecular mechanisms in aging mice
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STAT1 Drives the Interferon-Like Response and Aging Hallmarks in Progeria
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Insights into the therapeutic strategies for aging and aging-associated diseases
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Navigating Lipodystrophy: Insights from Laminopathies and Beyond
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Antioxidant Senotherapy by Natural Compounds: A Beneficial Partner in Cancer Treatment
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The role of prelamin A post-translational maturation in stress response and 53BP1 recruitment
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Progeria: a perspective on potential drug targets and treatment strategies
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Pharmacological frontiers in senescence: Transforming senescence with drug repurposing
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Self-citationSterile inflammation in laminopathies
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Vascular smooth muscle cell aging: Insights from Hutchinson-Gilford progeria syndrome
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Self-citationRIPK1 and necroptosis role in premature ageing
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Cytokine Receptors and Their Ligands
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Aging and cancer: current understandings and future perspectives
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Progeria (Hutchinson-Gilford Syndrome): Literature Review and Clinical Case
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Impact of miR-181a on SIRT1 Expression and Senescence in Hutchinson–Gilford Progeria Syndrome
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Engineering the cartilage niche: Mimicking the microenvironment for functional outcomes
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The Roles of Macrophage Lineage Cells ( MLC s) in Brain Aging
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Vascular smooth muscle cell aging: Insights from Hutchinson-Gilford progeria syndrome
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Syndromes with Premature Ageing
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Aging research from bench to bedside and beyond: What we learned from Sammy Basso
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Self-citationThe current report on drug development focuses on “The new dimension” of cancer hallmarks
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Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortalityPreprint
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Molecular drivers of ageing and emerging longevity therapies
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Targeting RANKL Prevents Bone Loss, Improves Muscle Function and Extends Lifespan in Progeroid Mice
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Collaborating with AIProSaB —A researcher's perspective on patient advocacy for progeria
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- Authors
- Squarzoni, S., Schena, E., Sabatelli, P., Mattioli, E., Capanni, C., Cenni, V., D'Apice, M. R., Andrenacci, D., Sarli, G., Pellegrino, V., Festa, A., Baruffaldi, F., Storci, G., Bonafè, M., Barboni, C., Sanapo, M., Zaghini, A., & Lattanzi, G.
- Affiliations
- Istituto Ortopedico Rizzoli (IT)
- Tor Vergata Hospital Medical Genetics Laboratory Rome Italy
- University of Bologna (IT)
- Corresponding author
- Lattanzi, Giovanna
- ORCID
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2021-01
- Volume
- 20
- Issue
- 1
- Pages
- e13285-e13285
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC7811841
- OpenAlex
- W3119837224
- Cited by
- 72
- References
- 65
- Citations by year
- 2026: 10 · 2025: 13 · 2024: 16 · 2023: 13 · 2022: 12 · 2021: 8
- FWCI
- 3.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Aging Cell (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion, cc-by)
- Funders
- Progeria Research Foundation (2019‐76)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Keywords
- Hutchinson-Gilford progeria syndrome, interleukin-6, tocilizumab, premature aging, progeroid mice, DNA damage response, aortic lesions, kyphosis, inflammation, anti-aging therapy
- MeSH terms
- Aging, Animals, Humans, Progeria, Interleukin-6, Mice
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