ArticleNature communications2020
Age-dependent loss of adipose Rubicon promotes metabolic disorders via excess autophagy.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 95 citations in OpenAlex.
- Down-Regulation of TFEB With Defective Autophagy in the Susceptibility of Aging Kidneys to Septic Acute Kidney Injury.Aging cell · 2026Article
- The emerging role and therapeutic targeting of autophagy-lysosome pathway in the pathogenesis of Parkinson's disease.Translational neurodegeneration · 2026Review
- Rubicon modulates neuroimmune responses following traumatic brain injury.bioRxiv : the preprint server for biology · 2026Article
- S-nitrosoglutathione reductase GSNOR drives age-related obesity by promoting adipose tissue whitening through de-nitrosation of Beclin-1.Nature communications · 2026Article
- Sepsis-associated skeletal muscle wasting is ameliorated by pharmacological inhibition of the STAT3 signaling pathway in mice.Scientific reports · 2026Article
- Article
- Preservation of Autophagy May Be a Mechanism Behind Healthy Aging.Aging cell · 2025Article
- Therapeutic potential of traditional Chinese medicine and mechanisms for the treatment of type 2 diabetes mellitus.Chinese medicine · 2025Review
- Adipose tissue ageing: implications for metabolic health and lifespan.Nature reviews. Endocrinology · 2025Review
- Dual-targeted siRubicon delivery strategy triggers hepatocellular lipophagy for mitigating liver steatosis.Nature communications · 2025Article
- Unraveling the complexities of diet induced obesity and glucolipid dysfunction in metabolic syndrome.Diabetology & metabolic syndrome · 2025Review
- Cell-Type-Specific Autophagy in Human Leukocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Autophagy does not always decline with ageing.Nature cell biology · 2025Article
- DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages.Nature communications · 2025Article
- Rubicon, a Key Molecule for Oxidative Stress-Mediated DNA Damage, in Ovarian Granulosa Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Recent Progress inInternational journal of molecular sciences · 2025Review
- Sex-specific and cell-type-specific changes in chaperone-mediated autophagy across tissues during aging.Nature aging · 2025Article
- Targeting macroautophagy to combat neurodegenerative disease: strategies and considerations.Autophagy reports · 2025Review
- Autophagy across tissues of aging mice.PloS one · 2025Article
- Mitochondrial quality control: the real dawn of intervertebral disc degeneration?Journal of translational medicine · 2024Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The systemic decline in autophagic activity with age impairs homeostasis in several tissues, leading to age-related diseases. A mechanistic understanding of adipocyte dysfunction with age could help to prevent age-related metabolic disorders, but the role of autophagy in aged adipocytes remains unclear. Here we show that, in contrast to other tissues, aged adipocytes upregulate autophagy due to a decline in the levels of Rubicon, a negative regulator of autophagy. Rubicon knockout in adipocytes causes fat atrophy and hepatic lipid accumulation due to reductions in the expression of adipogenic genes, which can be recovered by activation of PPARγ. SRC-1 and TIF2, coactivators of PPARγ, are degraded by autophagy in a manner that depends on their binding to GABARAP family proteins, and are significantly downregulated in Rubicon-ablated or aged adipocytes. Hence, we propose that age-dependent decline in adipose Rubicon exacerbates metabolic disorders by promoting excess autophagic degradation of SRC-1 and TIF2.
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