2012年1月3日，据《每日科学》报道，硫化氢，一种臭名昭著的臭鸡蛋气味的气体，可能最终能挽回它的名誉。它可以减少肾细胞中由高糖诱导产生的蛋白质疤痕，得克萨斯大学健康科学中心圣安东尼奥的研究人员在《生物化学杂志》（Journal of Biological Chemistry）发表了他们的最新研究成果。
研究论文定于2012年年初出版。
"气体作为生物事件的调解员，这非常的有意思，"B.S. Kasinath说，医学博士、医学教授、圣安东尼奥医学院肾病学家。"我们发现，当我们添加硫氢化钠到暴露于高糖的肾细胞（一种物质，可以释放硫化氢）中时，它减少了能致肾脏瘢痕的基质蛋白的产生。"与该结论相一致的是，在1型或2型糖尿病小鼠内，肾脏中促进硫化氢产生的酶减少了， Kasinath博士和他的团队报道称。
肾脏中的瘢痕，称之为肾纤维化，是导致终末期肾病的核心缺陷。在美国近一半终末期肾脏病与糖尿病有关，糖尿病是血糖调节能力较弱为标志的一种疾病。
"我们已经找到一种方法能够减少基质蛋白的合成，这是糖尿病中一个很重要的问题，"Kasinath博士说。"因为这些研究仅局限于细胞，研究结果不宜被扩展外推到人类糖尿病肾病的治疗，他强调道。
这一发现为研究老鼠或其他动物模型铺平了道路。硫化氢的安全性和有效性都应该在肾脏疾病动物模型中进行测试，之后才能考虑人体试验。这种防范措施是必要的，因为硫化氢在较高浓度时，是一种有毒物质。
生物化学编辑将该团队的稿件选为每周论文，设为所有稿件中占1％的极具意义和重要性的研究稿件。生物化学期刊每年发表超过6600篇论文，其中大约只有50~100篇能够获此殊荣。
Hak Joo Lee博士，肾脏病科的博士后研究人员，是该研究的第一作者。 Kasinath博士，Barshop长寿和老年化健康科学中心的成员，是研究的通讯作者，表达了对该项研究的其他共同作者的贡献表示肯定。
这项工作由国家卫生研究院/国家糖尿病、消化道和肾脏疾病研究所（DK077295）以及一个美国退伍军人事务部授予首席研究员Kasinath博士的研究资助。（生物谷bioon.com）
doi:10.1074/jbc.M111.278325
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Hydrogen sulfide inhibits high glucose-induced matrix protein synthesis by activating AMP-activated protein kinase in renal epithelial cells
H. J. Lee, M. M. Mariappan, D. Feliers, R. C. Cavaglieri, K. Sataranatarajan, H. E. Abboud, G. Ghosh Choudhury, B. S. Kasinath.
Capsule: Background: If hydrogen sulfide regulates protein synthesis is not known. Results: In kidney cells, hydrogen sulfide inhibited high glucose-induced synthesis of proteins including matrix proteins by activating AMP-activated protein kinase and inhibiting events in mRNA translation. Conclusion: Hydrogen sulfide reduces high glucose stimulation of matrix protein synthesis in renal cells. Significance: Hydrogen sulfide induction may inhibit kidney matrix protein accumulation in diabetes. Abstract: Hydrogen sulfide, a signaling gas, affects several cell functions. We hypothesized that hydrogen sulfide modulates high glucose (HG, 30 mM) stimulation of ma-trix protein synthesis in glomerular epithelial cells (GECs). HG stimulation of global protein synthesis, cel-lular hypertrophy, and matrix laminin and type IV col-lagen content was inhibited by NaHS, a H2S donor. HG activation of mTOR complex1 (mTORC1), shown by phosphorylation of p70S6 kinase and 4E-BP1, was in-hibited by NaHS. HG recruited mTORC1 to promote key events in the initiation and elongation phases of mRNA translation: binding of eIF4A to eIF4G, reduc-tion in PDCD4 expression and inhibition of its binding to eIF4A, eEF2 kinase phosphorylation and dephos-phorylation of eEF2; these events were inhibited by NaHS. Role of AMPK, an inhibitor of protein synthesis, was examined. NaHS dose-dependently stimulated AMPK phosphorylation and restored AMPK phos-phorylation reduced by HG. Compound C, an AMPK inhibitor, abolished NaHS effect on events in mRNA translation as well as global and matrix protein synthe-sis. NaHS induction of AMPK phosphorylation was in-hibited by siRNA for Ca calmodulin kinase kinase beta (CaMKKbeta), but not LKB1, upstream kinases for AMPK; STO-609, a CaMKKbeta inhibitor, had the same effect. Renal cortical content of cystathionine beta synthase and cystathionine gamma lyase, hydrogen sulfide generating enzymes, was significantly reduced in mice with type 1 diabetes or type 2 diabetes, coinciding with renal hyper-trophy and matrix accumulation. Hydrogen sulfide is a newly identified modulator of protein synthesis in the kidney and reduction in its generation may contribute to kidney injury in diabetes.
