2020
DOI: 10.1016/j.exger.2020.110891
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Senoinflammation: A major mediator underlying age-related metabolic dysregulation

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Cited by 17 publications
(15 citation statements)
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References 147 publications
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“…In fact, ageing causes cellular and molecular changes in tissue homeostasis, and it is associated with telomere shortening as well as with a multi-component senescence-associated secretory phenotype (SASP), displaying pro-inflammatory cytokines, chemokines, extracellular matrix (ECM)-degrading proteins and other cell-cycle arrest signaling molecules [ 94 , 95 , 96 , 97 ]. All the above factors result in the progressive deterioration of the structure and function of any given organ at the tissue and cell levels [ 97 ]. CSC ageing leads to a senescent phenotype, and to a decreased ability to differentiate and to heal cardiac injuries.…”
Section: Conclusion and Future Perspectivesmentioning
confidence: 99%
“…In fact, ageing causes cellular and molecular changes in tissue homeostasis, and it is associated with telomere shortening as well as with a multi-component senescence-associated secretory phenotype (SASP), displaying pro-inflammatory cytokines, chemokines, extracellular matrix (ECM)-degrading proteins and other cell-cycle arrest signaling molecules [ 94 , 95 , 96 , 97 ]. All the above factors result in the progressive deterioration of the structure and function of any given organ at the tissue and cell levels [ 97 ]. CSC ageing leads to a senescent phenotype, and to a decreased ability to differentiate and to heal cardiac injuries.…”
Section: Conclusion and Future Perspectivesmentioning
confidence: 99%
“…Recent studies provide strong evidence suggesting an essential role of chronic inflammation in the pathogenesis of the above-mentioned ARDs [2][3][4]. In addition, genotoxic stress, which is a component of a wide variety of pathological conditions, not only causes extensive DNA damage but also activates pathways leading to chronic inflammation (the ERK, JNK, and p38 MAPK pathways) and transcription of pro-inflammatory cytokines (TNF-α, IL-1β, interleukin 6 (IL-6)), chemokines (interleukin 8 (IL-8)), adhesion molecules (VCAM-1, ICAM-1, P-, E-selectin), and other pro-inflammatory enzymes including iNOS and COX-2 [5]. This in turn leads to an elevated pro-inflammatory status that is likely to set the stage for increased vulnerability to many ARDs [6].…”
Section: Introductionmentioning
confidence: 99%
“…During aging, multiple cellular stresses such as inflammation, oxidative stress, and endoplasmic reticulum stress affect the central nervous system (CNS) [1][2][3][4]. In particular, elevated inflammatory responses in the brain are common during aging [1,5].…”
Section: Introductionmentioning
confidence: 99%