投稿系统
Therapeutic potential of gasotransmitters for cold stress-related cardiovascular disease
doi: 10.2478/fzm-2022-0002
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Abstract: Growing evidence has shown that exposure to low ambient temperature poses a huge challenge to human health globally. Actually, cold stress is closely associated with a higher incidence of cardiovascular morbidity and mortality in winter or in cold regions. Cellular and molecular mechanisms underlying cardiovascular complications in response to cold exposure have yet to be fully clarified. Considering that cold exposure is an important risk of cardiovascular complications, it is necessary to clarify the molecular mechanism of cold stress-induced cardiovascular diseases and to develop effective intervention strategies. Hydrogen sulfide (H2S), nitric oxide (NO), and carbon monoxide (CO) are wellknown gasotransmitters that are endogenously produced in many biological systems. Accumulating studies have demonstrated that these gasotransmitters play a critical role in a wide spectrum of physiological and/or pathophysiological processes by regulating numerous signaling pathways. These gas signal molecules are emerging as important players in cardiovascular homeostasis, and disruption of these gasotransmitters is critically implicated in cardiovascular anomalies, such as hypertension, atherosclerosis, myocardial ischemia, heart failure, and stroke. Also, evidence is emerging that H2S, NO, and CO may be involved in the pathologies of cold stress-induced cardiovascular ailments. In this review, we aim to highlight and discuss the recent advances towards the development of gasotransmitters-based therapeutics for cold stressrelated cardiovascular pathogenesis. We believe that the effects of H2S, NO, and CO on cardiovascular regulation under cold environment will attract tremendous interest in the near future as they serve as novel regulators of cardiovascular biology in cold environment.
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Key words:
- cold stress /
- cardiovascular diseases /
- hydrogen sulfide /
- nitric oxide /
- carbon monoxide
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Figure 1. Effects of cold temperature on cardiovascular response in heathy controls and patients with hypertension, heart failure, coronary artery disease
(A) In healthy controls, the cardiovascular responses are presented. (B) Cold induces dysregulation and increases the risk of cold-related cardiovascular events in subjects with hypertension, heart failure, and coronary artery disease.
Figure 2. The hypothesized mechanisms of cold exposure-induced cardiovascular disorders
(1) In response to cold exposure, activation of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS) is responsible for elevation of blood pressure. (2) Cold-air exposure inhibits the skin blood flow due to the vasoconstriction, along with increased urine voiding, dehydration, hemoconcentration, and hyperviscosity. (3) Cold stress is associated with endothelial dysfunction, as evidenced by reductions in nitric oxide (NO) and adiponectin in the vascular system. In addition, cold environment contributed to atherosclerosis by enhancing lipid deposition, plaque instability, and plaque disruption. (4) Plasma levels of endothelin-1 levels are upregulated during cold stress, triggering mitochondria dysfunction in cardiomyocytes. All above changes induced by cold exposure could drive the development and progression of hypertension, myocardial infarction, ischemic stroke, atherosclerosis, cardiac hypertrophy and cardiac dysfunction.
Figure 3. A proposed mechanism of myocardial injury induced by cold stress
Abnormal changes in oxidative products, impaired autophagy processes, induction of apoptosis-related proteins, and increased level of endothelin-1 in myocardium could synergistically result in pathological hypertrophy, interstitial fibrosis, ultrastructural damage and cardiac dysfunction during cold exposure.
Figure 4. Production and metabolism of NO
(1) The formation of NO is catalyzed by neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS) from L-Arginine. (2) NO induces the relaxation of vascular smooth via sGC/cGMP signaling, followed by activation of PKG that phosphorylates several targets including MLCP and Cav. (3) During the cytotoxic pathway, NO reacts with superoxide anion to generate ONOO−, a strong oxidant that promotes DNA damage and inflammation. (4) The purine catabolic enzyme XOR could reduce NO3− to NO, and NO3− could be scavenged through the urine route. (5) S-nitrosation is involved in NO signal transduction mechanisms. sGC, soluble guanylyl cyclase; cGMP, cyclic guanosine monophosphate; PKG, protein kinase G; MLCP, myosin light chain phosphatase; Cav, voltage-gated calcium (Ca2+) channels; XOR, xanthine oxidoreductase; NO, nitric oxide.
Figure 5. Production and metabolism of CO. HO-1 and HO-2 enzymes are able to degrade heme to yield CO, iron, and biliverdin
(1) Excessive CO could be exhaled from the mammalian lungs. (2) In the classical pathway, CO is mechanistically identical to NO signaling, that is, CO activates the sGC/cGMP/PKG pathway that elicits smooth muscle relaxation. (3) Also, CO binds to heme groups of (BKCa) and increases BKCa channel opening, this can also cause smooth muscle relaxation. HO, heme oxygenase; CO, carbon monoxide; sGC, soluble guanylyl cyclase; cGMP, cyclic guanosine monophosphate; PKG, protein kinase G; MLCP, myosin light chain phosphatase; Cav, voltage-gated calcium (Ca2+) channels; NO, nitric oxide; BKCa, Ca2+-gated large conductance K+ channels.
Figure 6. Production and metabolism of H2S
Three enzymes can enzymatically produce H2S, CBS, CSE and 3-MST. With the aid of L-cysteine, CBS and CSE produce H2S. In an alternative pathway, 3-mercaptopyruvate could be produced by CAT using L-cysteine and DAO using D-cysteine, respectively. Then, 3-MST could generate H2S using 3-MP as the substrate.
(1) H2S could be exhaled. (2) Interaction of hemoglobin with H2S results in the production of sulfhemoglobin. (3) H2S is oxidized to thiosulfate, together with the formation of sulfite and sulfate. (4) H2S is methylated into dimethylsulfide by thiol S-methyltransferase. H2S, hydrogen sulfide; CBS, cystathionine β-synthase; CSE, cystathionine γ-lyase; 3-MST 3-mercaptopyruvate sulphurtransferase; 3-MP, 3-mercaptopyruvate; CAT, cysteine aminotransferase; DAO, D-amino acid oxidase. -
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