Glioblastoma, an aggressive primary malignant astrocytoma representing the most aggressive tumor of the central nervous system, suffers from a very poor prognosis, with recently reported 1‐year and 5‐year survival rates of 40.8% and 6.8%, respectively.¹ While glioblastoma patients initially respond well to surgery and conventional treatment strategies such as radiotherapy and chemotherapy, relapse and the development of resistance mechanisms often occur. The severity of glioblastoma derives partly from its highly infiltrative and migratory nature, as well as extensive cellular heterogeneity and plasticity.² Furthermore, the critical implication of glioma stem cells (GSCs) in glioblastoma initiation, progression, therapy resistance, relapse, and metastasis represents yet another complication.^{3, 4} As with other tumor types that involve cancer stem cells, targeting this specific cell population with advanced therapeutic approaches may represent an efficient means to halt glioblastoma development, inhibit metastatic spread, and significantly improve patient outcomes. Exciting research has also provided evidence that stem cell‐based therapies may also benefit glioblastoma patients, as the inherent tumor tropism observed in many stem cell populations can be taken advantage of to efficiently deliver therapeutic payloads to tumors. In the first of our Featured Articles published this month in STEM CELLS, Sareddy et al report that the specific activation of the estrogen receptor β (ERβ) reduces viability, inhibits self‐renewal, and increases apoptosis in GSCs and so may improve overall survival in glioblastoma patients.⁵ In a Related Article published recently in STEM CELLS Translational Medicine, Birbrair et al described tumor‐tropic neural‐like stem cells isolated from skeletal muscle tissue that can be engineered to carry therapeutic cargoes as a potentially effective approach to glioblastoma treatment.⁶

The regulation of blood pressure, fluid homeostasis, and overall cardiovascular physiology represents the principal function of the critical hormonal system known as the renin‐angiotensin system (or RAS). Briefly, a reduction in blood volume or a drop in blood pressure prompts the elevated secretion of the protease renin from cells within the kidney into the bloodstream, where it converts the polypeptide precursor angiotensinogen, which is synthesized in the liver, into angiotensin I. Subsequently, the angiotensin‐converting enzyme (ACE) present on the surface of vascular endothelial cells then cleaves angiotensin to form the potent vasoconstrictor angiotensin II, which functions through the type 1 and 2 receptors (AT1R and AT2R) to cause blood vessels to narrow and blood pressure to rise.⁷ In addition to the critical systemic effects described, a range of studies have also described the crucial role of local renin‐angiotensin systems in sites that include cardiac, vascular, and renal tissues,^{8, 9} where angiotensin peptides function as growth factors or inhibitors in a similar manner to cytokines. In the second of our Featured Articles published this month in STEM CELLS, Birbrair et al establish the importance of a local active renin‐angiotensin system to the emergence of undifferentiated hematopoietic stem/progenitor cells in the developing mouse and human embryo.¹⁰ In a Related Article published recently in STEM CELLS Translational Medicine, Kim et al provide evidence for the angiotensin II‐mediated death of hippocampal neural stem cells (NSCs) as a cause for heart failure‐associated memory impairment in a study that may aid the identification of novel therapeutic targets.¹¹

胶质母细胞瘤是一种侵袭性原发性恶性星形细胞瘤，是中枢神经系统最具侵袭性的肿瘤，预后极差，最近报道的 1 年和 5 年生存率分别为 40.8% 和 6.8%。¹虽然胶质母细胞瘤患者最初对手术和放疗和化疗等常规治疗策略反应良好，但经常发生复发和耐药机制的发展。胶质母细胞瘤的严重性部分源于其高度浸润性和迁移性，以及广泛的细胞异质性和可塑性。²此外，胶质瘤干细胞 (GSC) 在胶质母细胞瘤的发生、进展、治疗抵抗、复发和转移中的重要意义代表了另一种并发症。^{3, 4}与涉及癌症干细胞的其他肿瘤类型一样，用先进的治疗方法靶向这一特定细胞群可能是阻止胶质母细胞瘤发展、抑制转移扩散并显着改善患者预后的有效手段。令人兴奋的研究还提供了证据，表明基于干细胞的疗法也可能使胶质母细胞瘤患者受益，因为可以利用在许多干细胞群中观察到的固有肿瘤趋向性来有效地向肿瘤提供治疗有效载荷。在本月发表在STEM CELLS 上的第一篇精选文章中, Sareddy 等人报告称，雌激素受体 β (ERβ) 的特异性激活降低了 GSC 的活力、抑制了自我更新并增加了 GSC 的凋亡，因此可能会提高胶质母细胞瘤患者的总体生存率。⁵在最近发表在STEM CELLS Translational Medicine 上的一篇相关文章中，Birbrair 等人描述了从骨骼肌组织中分离出的嗜肿瘤性神经样干细胞，这些干细胞可以被设计为携带治疗性物质，作为治疗胶质母细胞瘤的潜在有效方法。⁶

血压、体液稳态和整体心血管生理的调节代表了称为肾素-血管紧张素系统（或 RAS）的关键激素系统的主要功能。简而言之，血容量减少或血压下降会促使肾脏内细胞分泌蛋白酶肾素增加进入血流，在那里它将在肝脏中合成的多肽前体血管紧张素原转化为血管紧张素 I。 随后, 血管内皮细胞表面的血管紧张素转换酶 (ACE) 然后裂解血管紧张素形成有效的血管收缩剂血管紧张素 II, 它通过 1 型和 2 型受体 (AT1R 和 AT2R) 起作用，导致血管变窄和血液流动。上升的压力。⁷除了所描述的关键全身效应外，一系列研究还描述了局部肾素 - 血管紧张素系统在包括心脏、血管和肾组织在内的部位的关键作用，^{8, 9}在这些部位，血管紧张素肽作为生长因子或抑制剂发挥作用。类似于细胞因子的方式。在我们本月发表在STEM CELLS 上的第二篇专题文章中，Birbrair 等人确定了局部活性肾素-血管紧张素系统对发育中的小鼠和人类胚胎中未分化造血干/祖细胞出现的重要性。¹⁰在最近发表在STEM CELLS Translational Medicine 上的相关文章中, Kim 等人在一项可能有助于确定新治疗靶点的研究中提供证据，证明血管紧张素 II 介导的海马神经干细胞 (NSC) 死亡是导致心力衰竭相关记忆障碍的原因。¹¹