Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Purpose: To explore differentially expressed genes (DEGs) associated with autophagy in psoriasis using bioinformatics analysis and verify them in an M5-induced psoriatic cell model.

Methods: We obtained gene expression microarray data from patients with psoriasis and normal skin tissues from the dataset GSE78097 of the NCBI Gene Expression Omnibus (GEO) database. R software was used to identify DEGs associated with autophagy in psoriasis. Proteinprotein interaction (PPI) and correlation analyses were used to show interactions between certain genes. Their potential biological roles were determined using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Finally, all the DEGs associated with autophagy in psoriasis were validated in a psoriatic cell model by RT-qPCR.

Results: 28 DEGs associated with autophagy were identified. These genes were linked to one another, and the most connected hub gene was , according to PPI analysis. GO and KEGG enrichment analyses revealed various biological pathways associated with autophagy. The RT-qPCR findings of the expression of 18 genes in the psoriatic cell model confirmed the bioinformatics analysis results. The five genes with the most significant differences were , and .

Conclusion: We identified DEGs associated with autophagy in patients with psoriasis. and were identified as important genes that may influence psoriasis development through the regulation of autophagy.

Download full-text PDF

Source
http://dx.doi.org/10.2174/0113862073238968230920054712DOI Listing

Publication Analysis

Top Keywords

associated autophagy
24
degs associated
20
autophagy psoriasis
12
psoriatic cell
12
genes
8
bioinformatics analysis
8
gene expression
8
patients psoriasis
8
kegg enrichment
8
enrichment analyses
8

Similar Publications

HMGB1: a multifaceted mediator of cell death pathways in cardiovascular diseases.

Apoptosis

September 2025

Department of Physiology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, Sichuang, China.

Cardiovascular diseases (CVDs) are a leading cause of death globally, responsible for 32% of all fatalities. They significantly reduce quality of life and life expectancy, while imposing a substantial economic burden on healthcare systems in different countries. High mobility group box 1 (HMGB1), a location-dependent multifunctional protein, plays a significant role in various cell death pathways associated with CVDs.

View Article and Find Full Text PDF

Background: Esophageal squamous cell carcinoma (ESCC) represents an aggressive cancer type associated with poor prognosis, often treated with neoadjuvant chemotherapy (NAC) using cisplatin-based regimens. However, cisplatin resistance limits therapeutic efficacy, necessitating a deeper understanding of resistance mechanisms. L-type amino acid transporter 1 (LAT1) plays a crucial role in amino acid uptake and is linked to cancer cell survival through activation of the mammalian target of rapamycin (mTOR) pathway.

View Article and Find Full Text PDF

Immune checkpoint inhibitors (ICIs) can re-active the immune response and induce a complete response in mismatch repair-deficient and microsatellite instability-high (dMMR/MSI-H) colorectal cancer (CRC). However, most CRCs exhibit proficient mismatch repair and microsatellite stable (pMMR/MSS) phenotypes with limited immunotherapy response because of sparse intratumoral CD8 T-lymphocyte infiltration. Cellular senescence has been reported to involve immune cell infiltration through a senescence-associated secretory phenotype (SASP).

View Article and Find Full Text PDF

Graphene oxide and its derivatives have unique physical and chemical properties with applications in many different fields. However, their biological effects and mechanisms of intracellular toxicity have not been completely clarified. In this study, we investigated the cytotoxic and autophagic activities of graphene oxide and its derivatives in A549 human lung carcinoma cells.

View Article and Find Full Text PDF

Counteracting lysosome defects alleviates the cellular senescence of Hutchinson-Gilford progeria syndrome.

Sci China Life Sci

September 2025

The Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.

Hutchinson-Gilford progeria syndrome (HGPS) is a rare progeroid disorder, and approximately 90% of cases are caused by LMNA mutation that yields the lamin A/C variant progerin. Progerin is toxic, and its clearance and disruption have positive benefits on HGPS cells and mice and even HGPS patients. However, accelerating progerin clearance is still an unaddressed issue.

View Article and Find Full Text PDF