The Proteostasis Network: Preserving Cellular Balance in Aging - Essay Sample

Introduction

The loss of proteostasis is prevalent in aging characterized by the formation of nonnative proteins that aggregate in the body but suppressed by the proteostasis network.Introduction

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'Loss of proteostatic checkpoint in intestinal stem cells' is an article that elaborates how the protein Homeostatic encompasses the balance between folding, degradation, re-folding, and protein to preserve the functions of cells and tissues for long-term purposes. Usually, it is the role of the Somatic stem cells to maintain the proteostatic capacity by making the cells supports their ability (Nat Commun, 2019 n.p). A proteostatic checkpoint is when there is a breakdown of the Somatic Cells following the coordination of the cell cycle after the proteins are arrested after the clearance of the Atg8. The balance is then permuted through the aging systems due to the high metabolic and oxidative stress.

Dysfunction of Mitochondrial

The figure shows how the proteins change their degradation machinery due to the control of proteolytic mechanisms. Later the Nrf2 is then activated to factor in the cap-n-collar, which consist of the cell cycle inhibitor as well as the proteolytic and Dacapo genes (Nat Commun, 2019 n.p). The decline in age, particularly in proteostatistics later strikes a balance due to the production of the prone proteins after a decade. This means that the Somatic Stem Cells are related to the intestinal barrier dysfunction that reduces the lifespan of a person because it affects the biology of the somatic stem cells due to their quality control mechanisms.

The Aim

Even though various studies have revealed the uniqueness of proteostatic regulation and capacity in the SCs, this study aims to show how SC's regenerative capacity and activity is linked to the proteolytic machinery, and how specific mechanisms found in SC's make sure that the homeostasis is preserved (Nat Commun. 2019 n.p). Drosophila intestinal stem cells are model systems that constitute to the competence of the mitotically cells found in the intestinal epithelium by regenerating different cells in response to the tissue damage (Kaser, Flak, Tomczak, Blumberg, 2015). Other studies have also discovered that multiple signalling pathways also regulate ISC self-renewal and proliferation.

Usually, when someone gets old, the intestinal epithelium refuses to function and begins to exhibit mis-differentiation and hyperplasia of the daughter and ISCs cells. This shows that age is related to the loss of the homeostasis due to the association of the inflammatory conditions facilitated by the chronic innate immune activation, increased oxidative stress, and commensal dysbiosis (Ryoo & Steller, 2017 p. 833). Further research also showed that the loss of proteostatic capacity is generated from constitutive activation of the proteins that are unfolded under the response of the endoplasmic reticulum (Harding, Zhang, Zeng, Novoa, et al. 2016 p. 624). In other words, the reduction of the ISCs extends lifespan and promotes homeostasis.

The Findings

The findings of the paper show that SCs have mechanisms that help to highlight the potential intervention strategies as well as to preserve the proteostasis to ensure that the regenerative homeostasis is maintained. The findings also show that since there is loss of the proteostatic checkpoint when it comes to the efficiency of the ISCs, they remain relevant to the homo preservations, particularly to the SCs vertebrates in adults (Heijmans, van Lidth de Jeude, Koo, Rosekrans, Wielenga, et al. 2015 p.1134). The importance of the findings to this study is that the activation of the cells turns to be an intervention strategy to maintain and improve the regenerative capacity when there is high tissue turn over in ageing individuals.

These findings imply that the ISCs responds to the ER-localized proteostatic or the cytosolic due to the stress that causes consequences for the understanding of tissue homeostasis. Even though the ISC is stimulated through the activation of JNK and PERK it also speculates prolific fiction of the unfolded proteins to allow the ISCs and ER to go through mitosis without having misregulations (Heijmans, van Lidth de Jeude, Koo, Rosekrans, Wielenga, et al. 2015 p. 1137). It is, therefore, tempting when someone thinks that the unfolded proteins activate the proteasome and autography of the pathways to assist clearing the cytosolic which aggregates with the incompatibility of the paths when the cell cycle increases the ISCs.

According to Adolph, Tomczak, Niederreiter, Ko H-J, Bock, et al. (2018 p. 274), the importance of proteostasis showed that the murine models and the C.elegans accumulate in the ER lumen and creates neurodegeneration (Walter & Ron, 2017 p.1083). This meant that the localization of the ER between the prominent neurodegeneration and the mutant neuroserpin created apoptotic pathways that stretched someone's aggregation once the proteins are expressed (Owusu-Ansah & Banerjee, 2019 p. 539). Other studies concluded that since SRP-2 and neuroserpin aggregate in the ER lumen, the relationship between the SCs and the protein aggregate became stronger. Interestingly, this happened because there was a genetic disruption between the branches of the central chaperones by increasing the polymeric and deposited forms.

Conclusion

The result to this study shows that ageing is a process that involves stressing the ER by inducing the proliferation of the ISC to make to activate the number of mitotic and how the functions develop consequences when the rate of symmetric division is increased due to the deficiency in SCs vertebrates in adults. Usually, it is the role of the Somatic stem cells to maintain the proteostatic capacity by making the cells supports their ability. Drosophila intestinal stem cells are model systems that constitute to the competence of the mitotically cells found in the intestinal epithelium by regenerating different cells in response to the tissue damage.

This means that these findings imply that the ISCs responds to the ER-localized proteostatic or the cytosolic due to the stress that causes consequences for the understanding of tissue homeostasis. Moreover, the localization of the ER between the prominent neurodegeneration and the mutant neuroserpin creates apoptotic pathways that stretched someone's aggregation once the proteins are expressed. Other studies concluded that since SRP-2 and neuroserpin aggregate in the ER lumen, the relationship between the SCs and the protein aggregate became stronger.

References

Adolph TE, Tomczak MF, Niederreiter L, Ko H-J, Bock J, et al. (2018) Paneth cells as a site of origin for intestinal inflammation. Nature 503: 272-276.

Harding HP, Zhang Y, Zeng H, Novoa I, Lu PD, et al. (2016) An integrated stress response regulates amino acid metabolism and resistance to oxidative stress. Mol Cell 11: 619-633.

Heijmans J, van Lidth de Jeude JF, Koo B-K, Rosekrans SL, Wielenga MCB, et al. (2015) ER Stress Causes Rapid Loss of Intestinal Epithelial Stemness through Activation of the Unfolded Protein Response. Cell reports 3: 1128-1139.

Kaser A, Flak MB, Tomczak MF, Blumberg RS (2015). The unfolded protein response and its role in intestinal homeostasis and inflammation. Experimental Cell Research 317: 2772-2779.

Nat Commun. (, 2019). Loss of a proteostatic checkpoint in intestinal stem cells contributes to age-related epithelial dysfunction

Owusu-Ansah E, Banerjee U (2019). Reactive oxygen species prime Drosophila hematopoietic progenitors for differentiation. Nature 461: 537-541

Ryoo HD, Steller H (2017) Unfolded protein response in Drosophila: why another model can make it fly. Cell Cycle 6: 830-835.

Walter P, Ron D (2017). The unfolded protein response: from stress pathway to homeostatic regulation. Science 334: 1081-1086.