Explaining Type 2 Diabetes with Transcriptomic Signatures of Pancreatic β-Cell Dysfunction and Death Induced by Human Islet Amyloid Polypeptide DOI
Pratiksha H. Roham,

Saurabh Singh Yadav,

B. Senthilnathan

et al.

OMICS A Journal of Integrative Biology, Journal Year: 2025, Volume and Issue: unknown

Published: April 22, 2025

Amyloid deposits formed by misfolding and aggregation of human islet amyloid polypeptide (hIAPP) are one the key pathophysiological features type 2 diabetes mellitus (T2DM) have been associated with loss function viability pancreatic β-cells. The molecular processes which hIAPP induces cytotoxicity in these cells not well understood. To best our knowledge, this is first report describing findings from combined analysis Affymetrix microarray high-throughput sequencing (HTS) Gene Expression Omnibus (GEO) datasets hIAPP-transgenic (Tg) mice islets. In brief, using GEO data, we compared silico islets obtained hIAPP-Tg wild-type mice. (GSE84423, GSE85380, GSE94672) HTS (GSE135276 GSE148809) were chosen. Weighted gene coexpression network was performed GSE135276 to identify coexpressed networks establish a correlation pattern between modules overexpression under hyperglycemic conditions. Subsequently, analyzed differential expression remaining datasets. Network hub genes pathways Cytoscape. Key present study include identification seven genes, namely, Ins2, Agt, Jun, Fos, CD44, Igf1, Ppar-γ, significantly involved process(es) insulin synthesis secretion, development resistance, oxidative stress, inflammation, mitophagy, apoptosis. conclusion, propose that can help explain T2DM pathogenesis be potentially utilized develop therapeutic interventions targeting for clinical management T2DM.

Language: Английский

Explaining Type 2 Diabetes with Transcriptomic Signatures of Pancreatic β-Cell Dysfunction and Death Induced by Human Islet Amyloid Polypeptide DOI
Pratiksha H. Roham,

Saurabh Singh Yadav,

B. Senthilnathan

et al.

OMICS A Journal of Integrative Biology, Journal Year: 2025, Volume and Issue: unknown

Published: April 22, 2025

Amyloid deposits formed by misfolding and aggregation of human islet amyloid polypeptide (hIAPP) are one the key pathophysiological features type 2 diabetes mellitus (T2DM) have been associated with loss function viability pancreatic β-cells. The molecular processes which hIAPP induces cytotoxicity in these cells not well understood. To best our knowledge, this is first report describing findings from combined analysis Affymetrix microarray high-throughput sequencing (HTS) Gene Expression Omnibus (GEO) datasets hIAPP-transgenic (Tg) mice islets. In brief, using GEO data, we compared silico islets obtained hIAPP-Tg wild-type mice. (GSE84423, GSE85380, GSE94672) HTS (GSE135276 GSE148809) were chosen. Weighted gene coexpression network was performed GSE135276 to identify coexpressed networks establish a correlation pattern between modules overexpression under hyperglycemic conditions. Subsequently, analyzed differential expression remaining datasets. Network hub genes pathways Cytoscape. Key present study include identification seven genes, namely, Ins2, Agt, Jun, Fos, CD44, Igf1, Ppar-γ, significantly involved process(es) insulin synthesis secretion, development resistance, oxidative stress, inflammation, mitophagy, apoptosis. conclusion, propose that can help explain T2DM pathogenesis be potentially utilized develop therapeutic interventions targeting for clinical management T2DM.

Language: Английский

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