Estimating the impact of drug addiction causes heart damage

Chang, Sheng-Huang; Pai, Peiying; Hsu, Chiung-Hung; Shibu, Marthandam Asokan; Tsai, Bruce Chi‐Kang; Weng, Wen-Tsan; Kuo, Wei‐Wen; Shih, Tien‐Tsorng; Kao, Hui-Chuan; Chen, William Shao‐Tsu; Huang, Chih‐Yang

doi:10.1080/01480545.2022.2122984

Cited by 3 publications

(1 citation statement)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Data are presented as means ± standard deviation. A significance level of p < 0.05 was considered statistically significant [ 24 , 25 ].…”

Section: Methodsmentioning

confidence: 99%

Development and evaluation of a novel chromium III-based compound for potential inhibition of emerging SARS-CoV-2 variants

Lin,

Sundhar,

Devi

et al. 2023

Heliyon

View full text Add to dashboard Cite

“…Data are presented as means ± standard deviation. A significance level of p < 0.05 was considered statistically significant [ 24 , 25 ].…”

Section: Methodsmentioning

confidence: 99%

Development and evaluation of a novel chromium III-based compound for potential inhibition of emerging SARS-CoV-2 variants

Lin,

Sundhar,

Devi

et al. 2023

Heliyon

View full text Add to dashboard Cite

Enhanced IGF‐IIRα Expression Exacerbates Lipopolysaccharide‐Induced Cardiac Inflammation, Hypertrophy, and Apoptosis Through Calcineurin Activation

Boonha,

Kuo,

Tsai

et al. 2024

Environmental Toxicology

View full text Add to dashboard Cite

Cardiovascular disease is one of the leading causes of death worldwide and has a high prevalence. Insulin‐like growth factor‐II receptor α (IGF‐IIRα) acts as a stress‐inducible negative regulator. This study focused on the substantial impact of heightened expression of IGF‐IIRα in cardiac myoblasts and its association with the exacerbation of cardiac dysfunction. Using lipopolysaccharide (LPS)‐induced H9c2 cardiac myoblasts as a model for sepsis, we aimed to elucidate the molecular interactions between IGF‐IIRα and LPS in exacerbating cardiac injury. Our findings demonstrated a synergistic induction of cardiac inflammation and hypertrophy by LPS stimulation and IGF‐IIRα overexpression, leading to decreased cell survival. Excessive calcineurin activity, triggered by this combined condition, was identified as a key factor exacerbating the negative effects on cell survival. Cellular changes such as cell enlargement, disrupted actin filaments, and upregulation of hypertrophy‐related and inflammation‐related proteins contributed to the overall hypertrophic and inflammatory responses. Overexpression of IGF‐IIRα also exacerbated apoptosis induced by LPS in H9c2 cardiac myoblasts. Inhibiting calcineurin in LPS‐treated H9c2 cardiac myoblasts with IGF‐IIRα overexpression effectively reversed the detrimental effects, reducing cell damage and mitigating apoptosis‐related cardiac mechanisms. Our study suggests that under sepsis‐like conditions in the heart with IGF‐IIRα overexpression, hyperactivation of calcineurin worsens cardiac damage. Suppressing IGF‐IIRα and calcineurin expression could be a potential intervention to alleviate the impact of the illness and improve cardiac function.

show abstract

Tannic Acid Impedes the Proliferation of Bladder Cancer Cells by Elevating Mitochondrial Pathways of Apoptosis

Li,

Tsai,

Annseles Rajula

et al. 2024

Cell Biochem Biophys

View full text Add to dashboard Cite

Estimating the impact of drug addiction causes heart damage

Cited by 3 publications

References 38 publications

Development and evaluation of a novel chromium III-based compound for potential inhibition of emerging SARS-CoV-2 variants

Development and evaluation of a novel chromium III-based compound for potential inhibition of emerging SARS-CoV-2 variants

Enhanced IGF‐IIRα Expression Exacerbates Lipopolysaccharide‐Induced Cardiac Inflammation, Hypertrophy, and Apoptosis Through Calcineurin Activation

Tannic Acid Impedes the Proliferation of Bladder Cancer Cells by Elevating Mitochondrial Pathways of Apoptosis

Contact Info

Product

Resources

About