T Cell Homeostatic Proliferation Promotes a Redox State That Drives Metabolic and Epigenetic Upregulation of Inflammatory Pathways in Lupus

Budd, Ralph C.; Scharer, Christopher D.; Barrantes-Reynolds, Ramiro; Legunn, Scott; Fortner, Karen A.

doi:10.1089/ars.2021.0078

Cited by 3 publications

(1 citation statement)

References 105 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Taken together, mitochondria are dynamic organelles and make great contributions in cellular maintaining homeostasis via regulation of the intracellular ROS and modulation of cell death programs (apoptosis triggered by cytochrome C) [ 119 , 120 ]. In type 2 diabetes, mitochondrial dynamics and mitochondrial biogenesis, as well as mitophagy were inhibited.…”

Section: Discussionmentioning

confidence: 99%

Mitophagy and mitochondrial dynamics in type 2 diabetes mellitus treatment

Zhao

Tian

et al. 2022

Aging

View full text Add to dashboard Cite

The prevalence of type 2 diabetes is associated with inflammatory bowels diseases, nonalcoholic steatohepatitis and even a spectrum of cancer such as colon cancer and liver cancer, resulting in a substantial healthcare burden on our society. Autophagy is a key regulator in metabolic homeostasis such as lipid metabolism, energy management and the balance of cellular mineral substances. Mitophagy is selective autophagy for clearing the damaged mitochondria and dysfunctional mitochondria. A myriad of evidence has demonstrated a major role of mitophagy in the regulation of type 2 diabetes and metabolic homeostasis. It is well established that defective mitophagy has been linked to the development of insulin resistance. Moreover, insulin resistance is further progressed to various diseases such as nephropathy, retinopathy and cardiovascular diseases. Concordantly, restoration of mitophagy will be a reliable and therapeutic target for type 2 diabetes. Recently, various phytochemicals have been proved to prevent dysfunctions of β-cells by mitophagy inductions during diabetes developments. In agreement with the above phenomenon, mitophagy inducers should be warranted as potential and novel therapeutic agents for treating diabetes. This review focuses on the role of mitophagy in type 2 diabetes relevant diseases and the pharmacological basis and therapeutic potential of autophagy regulators in type 2 diabetes.

show abstract

Section: Discussionmentioning

confidence: 99%

Mitophagy and mitochondrial dynamics in type 2 diabetes mellitus treatment

Zhao

Tian

et al. 2022

Aging

View full text Add to dashboard Cite

show abstract

Tissue damage in lupus

Nowling,

Oates

2025

Dubois' Lupus Erythematosus and Related Syndromes

View full text Add to dashboard Cite

ALKBH5 Expression could Affect the Function of T Cells in Systemic Lupus Erythematosus Patients: A Case-control Study

Deng

Fang

et al. 2022

CPD

View full text Add to dashboard Cite

Background: N6-methyladenosine (m6A) modification is widespread in eukaryotic mRNA, regulated by m6A demethylase, AlkB homolog 5 (ALKBH5). However, the role of m6A in systemic lupus erythematosus (SLE) is still obscure. We explored ALKBH5 expression in SLE patients and its effects on T cells. Methods: 100 SLE patients and 110 healthy controls were recruited to investigate the expression of ALKBH5 in peripheral blood mononuclear cells (PBMCs). An additional 32 SLE patients and 32 health controls were enrolled to explore the expression of ALKBH5 in T cells. Then we explored the function of ALKBH5 in T cells by lentivirus. Results: The expressions of ALKBH5 were downregulated in both PBMCs and T cells in SLE patients (all P<0.05). In PBMCs: ALKBH5 mRNA levels were associated with complement C4 level in plasma (P<0.05). In T cells: ALKBH5 mRNA levels were downregulated in SLE patients with low complement levels, high anti-dsDNA, anti-Sm, anti-RNP, and proteinuria compared with those without, respectively (all P<0.05); ALKBH5 mRNA levels were negatively related with SLE disease activity index score, erythrocyte sedimentation rate, and anti-dsDNA levels (all P<0.05), and positively correlated with complement C3 and C4 level (all P<0.05). Functionally, the overexpression of ALKBH5 promoted apoptosis and inhibited the proliferation of T cells (all P<0.05). Conclusion: Conclusion: ALKBH5 expression is downregulated in SLE patients and could affect the apoptosis and proliferation of T cells, but the exact mechanism still needs to be further explored.

show abstract

T Cell Homeostatic Proliferation Promotes a Redox State That Drives Metabolic and Epigenetic Upregulation of Inflammatory Pathways in Lupus

Cited by 3 publications

References 105 publications

Mitophagy and mitochondrial dynamics in type 2 diabetes mellitus treatment

Mitophagy and mitochondrial dynamics in type 2 diabetes mellitus treatment

Tissue damage in lupus

ALKBH5 Expression could Affect the Function of T Cells in Systemic Lupus Erythematosus Patients: A Case-control Study

Contact Info

Product

Resources

About