Overview on hydrogen sulfide-mediated suppression of vascular calcification and hemoglobin/heme-mediated vascular

Tamás Gáll1, Péter Nagy2, Dorottya Garai3

  • 1Division of Nephrology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Hungary; ELKH-UD Vascular Pathophysiology Research Group, 11003, University of Debrecen, Hungary; Kálmán Laki Doctoral School, University of Debrecen, Debrecen, Hungary.

Redox Biology
|October 14, 2022
PubMed

Insights

Hydrogen sulfide (H2S) may protect against atherosclerosis by inhibiting hemoglobin oxidation within plaques. This review explores H2S's beneficial effects on cardiovascular disease progression and vascular calcification.

Area of Science:

  • Biochemistry
  • Cardiovascular Research
  • Molecular Medicine

Background:

  • Hemorrhagic atherosclerotic plaques and calcified aortic valve disease (CAVD) significantly increase cardiovascular risk.
  • Red blood cell lysis releases hemoglobin (Hb), which oxidizes within plaques, promoting atherosclerosis.
  • Oxidized Hb and heme accumulation contribute to plaque instability and vascular calcification.

Purpose of the Study:

  • To review the effects of hydrogen sulfide (H2S) on atherosclerosis and CAVD.
  • To highlight H2S's role in mitigating Hb/heme oxidation within atherosclerotic plaques.
  • To explore H2S's potential therapeutic benefits in cardiovascular disease.

Main Methods:

  • Literature review focusing on studies investigating H2S, hemoglobin oxidation, and atherosclerosis.
  • Analysis of mechanisms by which cell-free Hb contributes to oxidative stress in plaques.
  • Examination of H2S's known physiological functions in vascular homeostasis.

Main Results:

  • Cell-free Hb undergoes oxidation to ferric and ferryl states, releasing heme and forming oxidized globin species.
  • Accumulation of methemoglobin (metHb) and ferryl-Hb is observed in atherosclerotic lesions.
  • Hydrogen sulfide (H2S) has demonstrated the ability to suppress pro-atherogenic cellular responses linked to Hb oxidation.

Conclusions:

  • H2S may offer protective effects against atherosclerosis by inhibiting Hb/heme oxidation.
  • Understanding H2S's role in vascular homeostasis is crucial for developing new therapeutic strategies.
  • H2S warrants further investigation for its potential in managing atherosclerosis and CAVD.

Related Concept Videos

Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
20
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
40
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
854
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
1.1K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.7K
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
24