Molecular basis of chronic inflammation in age-related diseases中西 真1) Omori S, Wang TW, Johmura Y, et al. Generation of a p16 Reporter Mouse and Its Use to Characterize and Target p16high Cells In Vivo. Cell Metab. 2020. 32(5):814-828.2) Johmura Y, Yamanaka T, Omori S, et al. Senolysis by glutaminolysis inhibition ameliorates various age-associated disorders. Science. 2021. 371(6526):265-270.3) Wang TW, Johmura Y, Suzuki N, et al. Blocking PD-L1-PD-1 improves senescence surveillance and aging phenotypes. Nature. 2022. 611(7935):358-364.4) Li D, Johmura Y, Morimoto S, et al. LONRF2 is a protein quality control ubiquitin ligase whose deficiency causes late-onset neurological deficits. Nature Aging. 2023. 3:1001-1019.5) Zhang Y, Wang TW, Tamatani M, et al. Signaling networks in cancer stromal senescent cells establish malignant microenvironment. Proc Natl Acad Sci U S A. 2025. 122(14):e2412818122.東京大学 医科学研究所 癌防御シグナル分野6. 慢性炎症による加齢病態の分子基盤The fundamental question of why and how humans age remains a subject of profound scientific and societal inquiry. This physiological phenomenon continues to be a significant enigma, with its underlying mechanisms remaining largely unexplained even in this era of scientific and technological advancement. However, it has become evident that the aging process varies among different species and is not a universal trait essential to life. Aging is a significant risk factor for numerous diseases, yet the underlying mechanisms remain elusive. Recent findings have revealed that the accumulation of inflammation-inducing cells and other inflammatory cells in organs with age, and their detrimental effects on the microenvironment, underlie organ dysfunction and disease development. The properties exhibited by these cells in vivo are determined by the organ in which they reside and the stimuli to which they are exposed1. It is widely accepted that many of these cells have deleterious effects on surrounding normal tissues. Notably, the elimination of inflammation-inducing cells from aging individuals has been demonstrated to reverse age-related organ dysfunction and various age-related diseases2,3. The presentation will introduce the recent findings of the molecular basis underlying age-dependent chronic inflammation and the technology that suppresses this detrimental condition4,5. Division of Cancer Cell Biology, The Institute of Medical Science, The University of Tokyo Makoto Nakanishi13
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