Insufficient S-sulfhydration of serum and glucocorticoid-regulated kinase 1 participates in hyperhomocysteinemia-induced liver injury.

Background & Aims: Previous studies have established that hyperhomocysteinemia (HHcy) significantly contributes to the development of non-alcoholic steatohepatitis (NASH). Conversely, hydrogen sulfide (HS) has shown potential in mitigating NASH. Despite these findings, it remains uncertain whether HS can serve as a therapeutic agent against HHcy-induced liver damage.

Nitration of cAMP-Response Element Binding Protein Participates in Myocardial Infarction-Induced Myocardial Fibrosis Accelerating Transcription of and .

Myocardial fibrosis after myocardial infarction (MI) leads to heart failure. Nitration of protein can alter its function. cAMP-response element binding protein (CREB) is a key transcription factor involved in fibrosis.

Cystathionine β-synthase is required for oocyte quality by ensuring proper meiotic spindle assembly.

Objectives: Poor oocyte quality is detrimental to fertilization and embryo development, which causes infertility. Cystathionine β-synthase (CBS) is one of the key enzymes modulating the metabolism of homocysteine (Hcy). Studies have shown that CBS plays an important role in female reproduction.

Upregulation of Periostin Through CREB Participates in Myocardial Infarction-induced Myocardial Fibrosis.

Myocardial fibrosis after myocardial infarction (MI) leads to heart failure, which has become an important global public health issue. One of the most important features of myocardial fibrosis is the abnormal deposition of extracellular matrix (ECM) proteins. Periostin is one of the ECM proteins.

Insufficient S-Sulfhydration of Methylenetetrahydrofolate Reductase Contributes to the Progress of Hyperhomocysteinemia.

Hyperhomocysteinemia (HHcy) has been considered as a risk factor for cardiovascular disease, Alzheimer's disease, nonalcoholic fatty liver, and many other pathological conditions. Vitamin B6, Vitamin B12, and folate have been used to treat HHcy in clinics. However, at present, clinical therapies of HHcy display unsatisfactory effects.

Abnormal nitration and S-sulfhydration modification of Sp1-CSE-HS pathway trap the progress of hyperhomocysteinemia into a vicious cycle.

Sp1-CSE-HS pathway plays an important role in homocysteine-metabolism, whose disorder can result in hyperhomocysteinemia. HS deficiency in hyperhomocysteinemia has been reported, while the underlying mechanism and whether it in turn affects the progress of hyperhomocysteinemia are unclear. This study focused on the post-translational modification of Sp1/CSE and revealed four major findings: (1) Homocysteine-accumulation augmented CSE's nitration, inhibited its bio-activity, thus caused HS deficiency.

Decreased autophagy of vascular smooth muscle cells was involved in hyperhomocysteinemia-induced vascular ageing.

Ageing and hyperhomocysteinemia (HHcy) are important risk factors for cardiovascular diseases (CVDs). HHcy affects the occurrence of vascular diseases in the elderly. So far, the mechanism of HHcy-induced vascular ageing remains largely unknown.

Nitrative Stress-Related Autophagic Insufficiency Participates in Hyperhomocysteinemia-Induced Renal Aging.

The kidneys are important organs that are susceptible to aging. Hyperhomocysteinemia (HHcy) is a risk factor for nephropathy and is associated with chronic nephritis, purpuric nephritis, and nephrotic syndrome. Numerous studies have shown that elevated serum homocysteine levels can damage the kidneys; however, the underlying mechanism of HHcy on kidney damage remains unclear.

β2-adrenergic receptor autoantibodies alleviated myocardial damage induced by β1-adrenergic receptor autoantibodies in heart failure.

Aims: β1-adrenergic receptor autoantibodies (β1-AAs) and β2-adrenergic receptor autoantibodies (β2-AAs) are present in patients with heart failure (HF); however, their interrelationship with cardiac structure and function remains unknown. This study explored the effects of the imbalance between β1-AAs and β2-AAs on cardiac structure and its underlying mechanisms in HF.

Methods And Results: Patients with left systolic HF who suffered from coronary heart disease (65.