ArticleAging cell2022
Accumulation of systematic TPM1 mediates inflammation and neuronal remodeling by phosphorylating PKA and regulating the FABP5/NF-κB signaling pathway in the retina of aged mice.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Retinal proteomics in neurodegeneration: Insights into ocular and brain disorders.Neural regeneration research · 2026Article
- Long-Read Single-Cell RNA Sequencing Reveals Dynamic Isoform Changes During Corneal Epithelial Wound Healing in Cynomolgus Monkeys.Investigative ophthalmology & visual science · 2026Article
- Prenatal acoustic communication triggers adaptive vascular programming in the developing avian brain.The Journal of experimental biology · 2026Article
- RANKL Inhibition and the Risk of Ocular Hypertension and Primary Open-Angle Glaucoma.Investigative ophthalmology & visual science · 2026Observational
- TPM1 drives cytoskeleton-immunometabolism coupling and LGALS9/CD45-mediated neuroinflammatory propagation in retinitis pigmentosa.Science advances · 2026Article
- Microglial CX3CR1 deficiency regulates the selective vulnerability of cone photoreceptors via STAT3/CCL-ACKR1 signaling in the mouse retina.Experimental & molecular medicine · 2026Article
- Targeting the CCL7-STAT1 axis attenuates microglial neurotoxicity and photoreceptor degeneration in retinitis pigmentosa.Journal of neuroinflammation · 2026Article
- Retinal Amyloid Clearance Enhanced by 40-Hz Light Flicker via MHC-II+ Microglia Regulation in Mice.Investigative ophthalmology & visual science · 2026Article
- Temporal biphasic regulation of photoreceptor degeneration by microglial TREM2: A metabolic-immune nexus in retinitis pigmentosa.Science advances · 2025Article
- Heterochronic parabiosis uncovers AdipoR1 as a critical player in retinal rejuvenation.Science advances · 2025Article
- New Insights into the Role of Cellular Senescence and Its Therapeutic Implications in Ocular Diseases.Bioengineering (Basel, Switzerland) · 2025Review
- High-fat stimulation induces atrial structural remodeling via the TPM1/P53/SHISA5 Axis.Lipids in health and disease · 2025Article
- Article
- RNAs mHeliyon · 2024Article
- Aging insights from heterochronic parabiosis models.npj aging · 2024Review
- Senolytic and senomorphic agent procyanidin C1 alleviates structural and functional decline in the aged retina.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Single-cell sequencing analysis and multiple machine-learning models revealed the cellular crosstalk of dendritic cells and identified FABP5 and KLRB1 as novel biomarkers for psoriasis.Frontiers in immunology · 2024Article
- Back pain exercise therapy remodels human epigenetic profiles in buccal and human peripheral blood mononuclear cells: an exploratory study in young male participants.Frontiers in sports and active living · 2024Article
- Comprehensive analysis of skin growth-related hub genes and microenvironment characterization in a mouse expanded skin model.Frontiers in immunology · 2024Article
- The rod synapse in aging wildtype and Dscaml1 mutant mice.PloS one · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms underlying functional decline during normal brain aging are poorly understood. Here, we identified the actin-associated protein tropomyosin 1 (TPM1) as a new systemic pro-aging factor associated with function deficits in normal aging retinas. Heterochronic parabiosis and blood plasma treatment confirmed that systemic factors regulated age-related inflammatory responses and the ectopic dendritic sprouting of rod bipolar (RBC) and horizontal (HC) cells in the aging retina. Proteomic analysis revealed that TPM1 was a potential systemic molecule underlying structural and functional deficits in the aging retina. Recombinant TPM1 protein administration accelerated the activation of glial cells, the dendritic sprouting of RBCs and HCs and functional decline in the retina of young mice, whereas anti-TPM1 neutralizing antibody treatment ameliorated age-related structural and function changes in the retina of aged mice. Old mouse plasma (OMP) induced glial cell activation and the dendritic outgrowth of RBCs and HCs in young mice, and yet TMP1-depleted OMP failed to reproduce the similar effect in young mice. These results confirmed that TPM1 was a systemic pro-aging factor. Moreover, we demonstrated that systematic TPM1 was an immune-related molecule, which elicited endogenous TPM1 expression and inflammation by phosphorylating PKA and regulating FABP5/NF-κB signaling pathway in normal aging retinas. Interestingly, we observed TPM1 upregulation and the ectopic dendritic sprouting of RBCs and HCs in young mouse models of Alzheimer's disease, indicating a potential role of TPM1 in age-related neurodegenerative diseases. Our data indicate that TPM1 could be targeted for combating the aging process.
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