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+{
+  "titles": [
+    "2018 -  Mechanisms of Vascular Aging.pdf",
+    "2017 - The Aging Cardiovascular System.pdf",
+    "2018 -  Mechanisms of Vascular Aging.pdf",
+    "2018 -  Mechanisms of Vascular Aging.pdf",
+    "2022 - Proteomic analysis reveals that aging rabbit.pdf",
+    "2022 - Proteomic analysis reveals that aging rabbit.pdf",
+    "2018 -  Mechanisms of Vascular Aging.pdf",
+    "2016 - The genome-wide role of HSF-1.pdf",
+    "2019 - Downregulation of miR-542-3p promotes.pdf",
+    "2007 - Sex-specific regulation of gene expression in the aging monkey aorta.pdf"
+  ],
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+    "208 Additional features that contribute to increased ar - terial stiffness include decreased elastin synthesis, elastin degradation and fragmentation, elastin calcification, al-terations in cross-linking of extracellular matrix compo-nents (eg, by increased presence of advanced glycation end products). 208,210,211 The pathophysiological consequences of age-related  ECM remodeling and arterial stiffening have been the sub-ject of a recent comprehensive review by AlGhatrif and Lakatta.",
+    "collagen. AGE-mediated cross-links can confer resis-tance to enzymatic degradation, and thus interferewith collagenolysis (56). In addition, increased ac- tivity of TGF- bwith aging stimulates the synthesis of interstitial collagen by vascular smooth muscle cells(VSMCs), and thereby augments arterial stiffness (57). Likewise, increased activity of the RAAS may augment collagen synthesis and heighten elastolysis (58). Endothelial dysfunction and arterial stiffness are",
+    "that many of these age-related ECM alterations are governed by circulating factors and factors produced in the vascular wall, including the extended renin-angiotensin-aldosterone system (see above) and an age-related decline in circulating IGF-1. 209 Collagen synthesis is also dysregulated with age in the  vascular wall likely because of the effects of increased para-crine action of TGF-  (transforming growth factor- ), 123  which contributes to vascular fibrosis and arterial stiffen-ing.",
+    "Ungvari et al  Mechanisms of Vascular Aging  859 Role of Extracellular Matrix Remodeling in  Vascular Aging The extracellular matrix (ECM) is an important contribu- tor to health and longevity. This noncellular compartment, ubiquitous to all tissues and organs does not only provide es-sential mechanical scaffolding but mediates highly dynamic  biomechanical and biochemical signals required for tissue  homeostasis, morphogenesis, and cell differentiation. Studies",
+    "1996;25(3):20915.  79. Bonnans C, Chou J, Werb Z. Remodelling the extracellular matrix in  development and disease. Nat Rev Mol Cell Biol. 2014;15(12):786801.  80. Swift J, Ivanovska IL, Buxboim A, Harada T, Dingal PCDP , Pinter J, et al.  Nuclear Lamin-A scales with tissue stiffness and enhances matrix- directed differentiation. Science. 2013;341(6149):1240104.  81. Vogel C, Marcotte EM. Insights into the regulation of protein abun- dance from proteomic and transcriptomic analyses. Nat Rev Genet.",
+    "result in extracellular matrix stiffness in aging larynx and  other organs [59, 79]. Finally, Lamin A was upregulated  by dehydration, by a smaller magnitude, especially when  observing the mean difference within the young groups.  Previous data has identified that Lamin proteins A and  C are important for imparting the nucleus with its stiff - ness, and their expression has been reported to scale with",
+    "aging. Annu Rev Biomed Eng. 2015;17:113141. doi: 10.1146/   annurev-bioeng-071114-040829  208. Jacob MP. Extracellular matrix remodeling and matrix metalloprotein- ases in the vascular wall during aging and in pathological conditions.  Biomed Pharmacother. 2003;57:195202.  209. Tarantini S, Valcarcel-Ares NM, Yabluchanskiy A, Springo Z, Fulop  GA, Ashpole N, Gautam T, Giles CB, Wren JD, Sonntag WE, Csiszar A,  Ungvari Z. Insulin-like growth factor 1 deficiency exacerbates hyperten-",
+    "able human diseases such as osteoporosis and musculo- skeletal diseases [53]. Collagens are long-lived proteins known to accumulate damage during aging, leading to a decline in tissue health [54]. Also, type I collagens be- come resistant to proteolysis upon age [55, 56], affecting their turnover. Interestingly, mice expressing cleavage- resistant type I collagen go through an accelerated aging process [57]. Thus, cellular aging can be affected by the state of the extracellular matrix in mammals.",
+    "the characteristics of endothelial dysfunction and pheno- typic transition of smooth muscle cells, resulting in in- creased vascular stiffness and increased thickness of vascular walls. It has been reported that the age- associated phenotypic transition of VSMCs is a crucial contributor to vascular remodeling [ 17,25]. However, the mechanism that drives phenotypic transition ofVSMCs with aging remains unclarified. In this study, using RNAs extracted from the in vitro cultured VSMCs,",
+    "downregulation with aging of genes involved in the synthesisof the ECM and in particular of different forms of collagen(Table 2). In addition, aging males but not females showed adecrease in collagen type III. Interestingly, collagen type IIIdecreases the size of collagen bundles and thereby increasesvascular elasticity (11). Therefore, a decreased expression ofcollagen type III can participate in the increased stiffness thatcharacterizes the aging aorta (23). An interesting observationfrom our study that"
+  ],
+  "answer": "Extracellular matrix (ECM) remodeling and tissue stiffness are significant factors in the aging process. As we age, several changes occur in the ECM that contribute to increased tissue stiffness. These changes include decreased elastin synthesis, elastin degradation and fragmentation, and alterations in the cross-linking of ECM components, such as increased presence of advanced glycation end products (AGEs) [1]. AGEs can interfere with collagenolysis by forming cross-links that confer resistance to enzymatic degradation, thereby contributing to increased arterial stiffness [2].  Additionally, the activity of transforming growth factor-beta (TGF-\u03b2) increases with age, stimulating the synthesis of interstitial collagen by vascular smooth muscle cells (VSMCs), which further augments arterial stiffness [2]. The renin-angiotensin-aldosterone system (RAAS) also plays a role in this process by augmenting collagen synthesis and promoting elastolysis [2].  The ECM is crucial for providing mechanical scaffolding and mediating biomechanical and biochemical signals necessary for tissue homeostasis and cell differentiation [4]. However, with aging, ECM stiffness increases, affecting various organs, including the larynx [6]. This increased stiffness is associated with a decline in tissue health, as seen with the accumulation of damage in long-lived proteins like collagens, which become resistant to proteolysis and affect their turnover [8].  Overall, these changes in ECM remodeling and tissue stiffness contribute to the aging process by affecting vascular and tissue elasticity, leading to conditions such as arterial stiffening and vascular remodeling [1], [3], [9].",
+  "question": "How are extracellular matrix remodeling and tissue stiffness implicated in the aging process?"
+}
+\ No newline at end of file