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The mutual regulation between hydrogen sulfide (H 2 S) and microRNA (miRNA) is involved in the development of many diseases, including cancer, cardiovascular disease, inflammatory disease, and high-risk pregnancy. Abnormal expressions of endogenous H 2 S-producing enzyme and miRNA in tissues and cells often indicate the occurrence of diseases, so the maintenance of their normal levels in the body can mitigate damages caused by various factors. Many studies have found that H 2 S can promote the migration, invasion, and proliferation of cancer cells by regulating the expression of miRNA, while many H 2 S donors can inhibit cancer progression by interfering with the proliferation, apoptosis, cell cycle, metastasis, and angiogenesis of cancer cells. Furthermore, the mutual regulation between H 2 S and miRNA can also prevent cell injury in cardiovascular disease and inflammatory disease through anti-inflammation, anti-oxidation, anti-apoptosis, and pro-autophagy. In addition, H 2 S can promote angiogenesis and relieve vasoconstriction by regulating the expression of miRNA, thereby improving fetal growth in high-risk pregnancy. In this review, we discuss the mechanism of mutual regulation between H 2 S and miRNA in various diseases, which may provide reliable therapeutic targets for these diseases., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2024 Elsevier Inc. All rights reserved.)

In recent years, the impact of age-related diseases on human health has become increasingly severe, and developing effective drugs to deal with these diseases has become an urgent task. Considering the essential regulatory role of hydrogen sulfide (H 2 S) in these diseases, it is regarded as a promising target for treatment. H 2 S is a novel gaseous transmitter involved in many critical physiological activities, including anti-oxidation, anti-inflammation, and angiogenesis. H 2 S also regulates cell activities such as cell proliferation, migration, invasion, apoptosis, and autophagy. These regulatory effects of H 2 S contribute to relieving and treating age-related diseases. In this review, we mainly focus on the pathogenesis and treatment prospects of H 2 S in regulating age-related diseases., Competing Interests: Declaration of competing interest The authors declare that they have no competing interests., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Hydrogen sulfide (H 2 S) has been identified as the third gaseous signaling molecule. Endogenous H 2 S plays a key role in the progression of various types of cancer. However, the effect of endogenous H 2 S on the growth of esophageal cancer (EC) remains unknown., Methods: In this study, three kinds of H 2 S-producing enzymes inhibitors, DL-propargylglycine (PAG, inhibitor of cystathionine-γ-lyase), aminooxyacetic acid (AOAA, inhibitor of cystathionine-β-synthase), and L-aspartic acid (L-Asp, inhibitor of 3-mercaptopyruvate sulfurtransferase) were used to determine the role of endogenous H 2 S in the growth of EC9706 and K450 human EC cells., Results: The results indicated that the combination (PAG+AOAA+L-Asp) group showed higher inhibitory effects on the viability, proliferation, migration, and invasion of EC cells than PAG, AOAA, and L-Asp group. Inhibition of endogenous H 2 S promoted apoptosis via activation of mitogen-activated protein kinase pathway in EC cells. Endogenous H 2 S suppression triggered pyroptosis of EC cells by activating reactive oxygen species-mediated nuclear factor-κB signaling pathway. In addition, the combine group showed its more powerful growth-inhibitory effect on the growth of human EC xenograft tumors in nude mice without obvious toxicity., Conclusion: Our results indicate that inhibition of endogenous H 2 S production can significantly inhibit human EC cell growth via promotion of apoptosis and pyroptosis. Endogenous H 2 S may be a promising therapeutic target in EC cells. Novel inhibitors for H 2 S-producing enzymes can be designed and developed for EC treatment., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflicts of interest related to this work., (Copyright © 2023. Published by Elsevier Inc.)

Background: To provide person-centered symptom management, the interindividual variability in breast cancer patients merits further exploration. However, how sociodemographic and clinical characteristics influence symptom profile membership in endocrine therapy for breast cancer is still unknown., Objectives: This study aimed to explore symptom profiles of breast cancer patients undergoing endocrine therapy and to identify sociodemographic and clinical characteristics among symptom subgroup members., Methods: A cross-sectional study was conducted, and participants were invited to complete a general information questionnaire and Functional Assessment of Cancer Therapy-Endocrine Subscale. Latent profile analysis, univariate analysis, and multinomial logistic regression were performed to explore symptom profiles and identify interindividual variability., Results: Three distinct subgroups were identified: "all high" (9.8%), "all moderate but high sexual symptoms" (25.4%), and "all low" (64.8%). Age, body mass index, main payment source for medical expenses, type of endocrine therapy, and history of breast cancer treatment were factors that determined membership in these 3 symptom subgroups., Conclusion: Patients' demographic and clinical characteristics were associated with their endocrine therapy-related symptom profiles. In general, those younger in age who pay out of pocket for medical expenses, use aromatase inhibitors, present a history of chemotherapy, and have a higher body mass index have a greater risk of symptom burden., Implication for Practice: The findings of this study will contribute to implementing individual cancer care based on the characteristics and needs of patient subgroups, which may improve the allocation of medical resources and provide interventions tailored to patients' unique needs., Competing Interests: The authors have no funding or conflicts of interest to disclose., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Hydrogen sulfide (H 2 S) has been widely recognized as one of gasotransmitters. Endogenous H 2 S plays a crucial role in the progression of cancer. However, the effect of endogenous H 2 S on the development of nasopharyngeal carcinoma (NPC) is still unknown. In this study, aminooxyacetic acid (AOAA, an inhibitor of cystathionine-β-synthase), dl-propargylglycine (PAG, an inhibitor of cystathionine-γ-lyase), and l-aspartic acid (l-Asp, an inhibitor of 3-mercaptopyruvate sulfurtransferase) were adopted to detect the role of endogenous H 2 S in NPC growth. The results indicated that the combine (PAG + AOAA + l-Asp) group had higher inhibitory effect on the growth of NPC cells than the PAG, AOAA, and l-Asp groups. There were similar trends in the levels of apoptosis and reactive oxygen species (ROS). In addition, the combine group exhibited lower levels of phospho (p)-extracellular signal-regulated protein kinase but higher expressions of p-p38 and p-c-Jun N-terminal kinase than those in the AOAA, PAG, and l-Asp groups. Furthermore, the combine group exerted more potent inhibitory effect on NPC xenograft tumor growth without obvious toxicity. In summary, suppression of endogenous H 2 S generation could dramatically inhibit NPC growth via the ROS/mitogen-activated protein kinase pathway. Endogenous H 2 S may be a novel therapeutic target in human NPC cells. Effective inhibitors for H 2 S-producing enzymes could be designed and developed for NPC treatment., (© 2023 Wiley Periodicals LLC.)

The role of hydrogen sulphide (H 2 S) in angiogenesis has been widely demonstrated. Vascular endothelial growth factor (VEGF) plays an important role in H 2 S-induced angiogenesis. H 2 S promotes angiogenesis by upregulating VEGF via pro-angiogenic signal transduction. The involved signalling pathways include the mitogen-activated protein kinase pathway, phosphoinositide-3 kinase pathway, nitric oxide (NO) synthase/NO pathway, signal transducer and activator of transcription 3 (STAT3) pathway, and adenosine triphosphate (ATP)-sensitive potassium (K ATP ) channels. H 2 S has been shown to contribute to tumour angiogenesis, diabetic wound healing, angiogenesis in cardiac and cerebral ischaemic tissues, and physiological angiogenesis during the menstrual cycle and pregnancy. Furthermore, H 2 S can exert an anti-angiogenic effect by inactivating Wnt/β-catenin signalling or blocking the STAT3 pathway in tumours. Therefore, H 2 S plays a double-edged sword role in the process of angiogenesis. The regulation of H 2 S production is a promising therapeutic approach for angiogenesis-associated diseases. Novel H 2 S donors and/or inhibitors can be developed in the treatment of angiogenesis-dependent diseases., (© 2022 The Authors. Cell Proliferation published by Beijing Institute for Stem Cell and Regenerative Medicine and John Wiley & Sons Ltd.)

Thyroid cancer is considered to be one of the most common endocrine tumors worldwide. Cystathionine β -synthase (CBS) plays a crucial role in the occurrence of several types of malignancies. And yet, the mechanism of action of CBS in the growth of thyroid carcinoma cells is still unrevealed. We found that CBS level in thyroid carcinoma tissue was higher than that in adjacent normal tissue. The overexpression of CBS enhanced the proliferation, migration, and invasion of thyroid cancer cells, while the downregulation of CBS exerted reverse effects. CBS overexpression reduced the levels of cleaved caspase-3 and cleaved poly ADP-ribose polymerase in thyroid cancer cells, whereas CBS knockdown showed reverse trends. CBS overexpression decreased reactive oxygen species (ROS) levels but increased the levels of Wnt3a and phosphorylations of phosphatidylinositol 3-kinase (PI3K), protein kinase B (PKB/AKT), mammalian target of rapamycin (mTOR), β -catenin, and glycogen synthase kinase-3 beta, while CBS knockdown exerted opposite effects. In addition, CBS overexpression promoted the growth of xenografted thyroid carcinoma, whereas CBS knockdown decreased the tumor growth by modulating angiogenesis, cell cycle, and apoptosis. Furthermore, aminooxyacetic acid (an inhibitor of CBS) dose-dependently inhibited thyroid carcinoma cell growth. CBS can regulate the proliferation, migration, and invasion of human thyroid cancer cells via ROS-mediated PI3K/AKT/mTOR and Wnt/ β -catenin pathways. CBS can be a potential biomarker for diagnosing or prognosing thyroid carcinoma. Novel donors that inhibit the expression of CBS can be developed in the treatment of thyroid carcinoma., Competing Interests: The authors declare that they have no competing interests., (Copyright © 2022 Qi-Ying Jiang et al.)

Hydrogen sulfide (H 2 S) has long been considered as a toxic gas, but as research progressed, the idea has been updated and it has now been shown to have potent protective effects at reasonable concentrations. H 2 S is an endogenous gas signaling molecule in mammals and is produced by specific enzymes in different cell types. An increasing number of studies indicate that H 2 S plays an important role in cardiovascular homeostasis, and in most cases, H 2 S has been reported to be downregulated in cardiovascular diseases (CVDs). Similarly, in preclinical studies, H 2 S has been shown to prevent CVDs and improve heart function after heart failure. Recently, many H 2 S donors have been synthesized and tested in cellular and animal models. Moreover, numerous molecular mechanisms have been proposed to demonstrate the effects of these donors. In this review, we will provide an update on the role of H 2 S in cardiovascular activities and its involvement in pathological states, with a special focus on the roles of exogenous H 2 S in cardiac protection.