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Implication of homocysteine in protein quality control processes
V Sudhakar Reddy1, Jamma Trinath2, G Bhanuprakash Reddy1
1Biochemistry Division, National Institute of Nutrition, Hyderabad, India.
Biochimie
|July 4, 2019
Summary
High homocysteine (HHcy) levels impair cellular protein quality control, contributing to cardiovascular and brain diseases. Vitamin B12 (cobalamin) deficiency exacerbates this, highlighting its therapeutic potential.
Area of Science:
- Biochemistry
- Cell Biology
- Neuroscience
Background:
- Homocysteine (Hcy) is a metabolite linked to cardiovascular and brain diseases when levels are elevated (hyperhomocysteinemia, HHcy).
- Vitamin B12 (cobalamin) deficiency is a cause of HHcy and is associated with hematological and neurological disorders.
- Cellular protein quality control (PQC) maintains proteome integrity, and its failure contributes to disease.
Purpose of the Study:
- To review the impact of HHcy on cellular PQC mechanisms.
- To explore the pathophysiological and clinical consequences of HHcy-induced PQC dysfunction.
- To discuss the therapeutic potential of Vitamin B12 and chemical chaperones.
Main Methods:
- Review of existing literature on HHcy, PQC, and related diseases.
- Analysis of cell culture and experimental animal models.
- Examination of molecular mechanisms including protein homocysteinylation and signaling pathways.
Main Results:
- HHcy perturbs PQC by reducing chaperone levels, activating the unfolded protein response (UPR), and impairing autophagy.
- HHcy induces cytotoxicity, inflammation, protein aggregation, and apoptosis.
- Altered SIRT1-HSF1 axis and protein homocysteinylation are implicated in HHcy-induced PQC impairment.
Conclusions:
- HHcy significantly disrupts cellular PQC, contributing to various diseases.
- Vitamin B12 (cobalamin) and chemical chaperones show therapeutic promise for HHcy-related conditions.
- Further research into HHcy's role in PQC is crucial for developing effective treatments.
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