Department of Pharmacy

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Author: search.filters.author.Chitkara, DeepakSubject: search.filters.subject.Autophagy

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    Autophagy as a potential therapeutic target in regulating improper cellular proliferation
    (Frontiers Media, 2025-05) Chitkara, Deepak
    Autophagy is a degradative process that makes rapid turnover of old and impaired proteins and organelles possible. It is highly instigated by stress signals, like starvation, and contributes to the cell’s homeostasis. Autophagy performs a crucial function in keeping cell genomic integrity stable. Impaired autophagic flux is implicated in neurodegenerative diseases, abnormal ageing, and cancerous diseases. In diseases like cancer, autophagy performs a dualistic function; it can have both a tumor-suppressive and supportive role. Autophagy in the initial phases of tumorigenesis maintains the integrity of the genome and, if it fails, leads to cell death, thus having a tumor-suppressive role. Meanwhile, autophagy also imparts the function of the pro-survival mechanism in the latter stages of tumorigenesis and supports the cancerous cells in surviving conditions like hypoxia and increased oxidative stress. Autophagy also helps cancerous cells develop drug resistance in some cases. Thus, modulation of the autophagic mechanism is a possible therapeutic strategy in cancer therapy as its inhibition can sensitise cancer cells to anti-cancerous drugs. The promotion of autophagy, in some cases, can also safeguard cells from toxic protein aggregation and enhanced oxidative stress. Excessive autophagy can result in autophagic cell death. Autophagy also regulates several cellular processes and cell death pathways, like apoptosis. Therefore, an in-depth knowledge of the autophagy process and its regulating molecules is critically important. Pharmaceutical small molecules or cellular target modulation can help modulate the cellular autophagy process in the context of specific disease conditions.
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    Proteostasis defects: Medicinal challenges of imperfect aging & neurodegeneration
    (Elsevier, 2023) Chitkara, Deepak
    A prolonged healthy life is based on the optimal activity of an organism’s organ systems, and healthy cells are at the core of this proper functioning. Cellular homeostasis is of utmost importance, and a cell deploys several cytoprotective mechanisms to maintain this balance. One such mechanism is protein quality control (PQC) to preserve proteostasis and maintain functionality of proteins. In PQC, the chaperone system and proteolytic pathways like autophagy and ubiquitin-proteasome system (UPS) are primary cell devices preventing misfolding/aggregation of proteins and clearing out toxic protein aggregates and dysfunctional organelles. Aging is an unavoidable biological phenomenon observed in many organisms that negatively affects the functionality of multiple organs systems, thus reducing the life span. It constitutes a significant risk factor for impairment of PQC elements and proteostasis disruption, linked with physiological dysfunction of organelles along with other anomalies. Aging presents various medicinal challenges as it affects multiple physiological processes at once. In aging, declined PQC capacity can lead to increased incidence of several age-associated diseases, including neurodegenerative disorders. Proper maintenance and modulation of these PQC elements present an attractive therapeutic intervention opportunity for such disorders. Here, we present PQC and its components as a system affected in imperfect aging, its potential for modulation to improve healthspan and counter aging associated disorders, along with challenges linked with inherent complex nature of aging biology.