Suneeta Kochhar, Marcia Excell

This article reviews a service pathway offering people attending their diabetes eye screening appointments an opportunistic blood pressure check to support hypertension case finding and treatment to target. The pathway promotes patient choice and facilitates primary and secondary care collaboration, as well as utilisation of home blood pressure readings. From the 200 participants in the study, 91 (45.5%) had clinic blood pressure readings above 140/90 mmHg, of whom 48 agreed to undertake home blood pressure monitoring. Of those, 33 individuals had elevated home blood pressure readings – 13 with newly diagnosed hypertension and 20 requiring treatment to target of their pre-existing hypertension. All 33 were contacted to ensure that they had been followed up by their GP practice. Participant feedback was positive.

Citation: Kochhar S, Excell M (2024) Hypertension case finding and treatment to target as part of the NHS diabetes eye screening programme. Diabetes & Primary Care 26: [Early view publication]

Article points

1. People attending their diabetes eye screening appointments may be offered an opportunistic blood pressure check to support case finding and treatment to target of hypertension.

2. Pathways for raised blood pressure may utilise home blood pressure readings to facilitate supported self-management.

3. Interface working with community providers/secondary care and primary care providers may result in early treatment of hypertension, and treatment to target is known to improve cardiovascular outcomes especially in people with diabetes.

Key words

– Cardiovascular disease

– Hypertension

– Service delivery

Authors

Suneeta Kochhar, GP Principal and Clinical Lead for CVD Prevention, NHS Sussex; Marcia Excell, RN, East Sussex Healthcare NHS Trust, and Chief Nurse Fellow, University Hospitals Sussex NHS Foundation Trust.

Highlights

● DSB repair, but not NER, coevolves with maximum lifespan (MLS) in rodents

● The activity of SIRT6 in stimulating DSB repair coevolves with MLS in rodent species

● Five amino acids determine the differential activities of mouse and beaver SIRT6

● Stronger SIRT6 leads to a longer lifespan

Authors

Xiao Tian, Denis Firsanov, Zhihui Zhang, ..., Vadim N. Gladyshev, Andrei Seluanov, Vera Gorbunova

Correspondence

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In Brief

A comparative analysis of 18 rodent species identifies a role for SIRT6-dependent DNA double strand break repair as a major factor in organismal lifespan

Xiao Tian,1 Denis Firsanov,1 Zhihui Zhang,1 Yang Cheng,2 Lingfeng Luo,1 Gregory Tombline,1 Ruiyue Tan,1 Matthew Simon,1 Steven Henderson,1 Janine Steffan,1 Audrey Goldfarb,1 Jonathan Tam,1 Kitty Zheng,1 Adam Cornwell,1 Adam Johnson,1 Jiang-Nan Yang,3 Zhiyong Mao,4 Bruno Manta,5 Weiwei Dang,6 Zhengdong Zhang,7 Jan Vijg,7 Aaron Wolfe,8 Kelsey Moody,8 Brian K. Kennedy,9,10 Dirk Bohmann,2 Vadim N. Gladyshev,5 Andrei Seluanov,1,* and Vera Gorbunova1,11,*

1 Department of Biology, University of Rochester, Rochester, NY 14627, USA

2 Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, NY 14642, USA

3 Leibniz Institute on Aging - Fritz Lipmann Institute, Beutenbergstraße 11, Jena D-07745, Germany

4 School of Life Sciences and Technology, Tongji University, Shanghai 200092, China

5 Division of Genetics, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA

6 Huffington Center on Aging, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA

7 Department of Genetics, Albert Einstein College of Medicine, Bronx, NY, USA

8 Ichor Therapeutics, 2521 US-11, Lafayette, NY 13084, USA

9 Departments of Biochemistry and Physiology, National University Singapore, Singapore

10 Centre for Healthy Aging, National University Health System, Singapore

11 Lead Contact

*Correspondence: 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (A.S.), 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (V.G.) https://doi.org/10.1016/j.cell.2019.03.043

Graphical Abstract

Highlights

● scRNA/CITE-seq and scATAC-seq reveal hallmarks of immune aging in mice and humans

● Clonal exhausted-like GZMK+ CD8+ T cells accumulate in tissues due to old environment

● GZMK secreted by activated GZMK+ CD8+ T cells can promote SASP from senescent cells

● GZMK+ CD8+ Taa rather than GZMB+ CD8+ Tem accumulate in human blood with age

Authors

      Denis A. Mogilenko, Oleg Shpynov, Prabhakar Sairam Andhey, ..., Sheila A. Stewart, Marco Colonna, Maxim N. Artyomov

Correspondence

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In Brief

      Aging affects the immune system and establishes a chronic low-grade inflammation (inflammaging). Mogilenko et al. defined organ-specific and common alterations of immune cell populations in aging and identified a distinct subset of clonal GZMK+ CD8+ T cells as a conserved cellular hallmark of inflammaging in mice and humans.

Denis A. Mogilenko,1 Oleg Shpynov,1,2,6 Prabhakar Sairam Andhey,1,6 Laura Arthur,1 Amanda Swain,1 Ekaterina Esaulova,1 Simone Brioschi,1 Irina Shchukina,1 Martina Kerndl,1,3 Monika Bambouskova,1 Zhangting Yao,4 Anwesha Laha,1 Konstantin Zaitsev,5 Samantha Burdess,1 Susan Gillfilan,1 Sheila A. Stewart,4 Marco Colonna,1 and Maxim N. Artyomov1,7, *

1 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA

2 JetBrains Research, Saint Petersburg 197374, Russia

3 Institute for Vascular Biology, Centre for Physiology and Pharmacology & Christian Doppler Laboratory for Arginine Metabolism in Rheumatoid Arthritis and Multiple Sclerosis, Vienna 1090, Austria

4 Department of Cell Biology and Physiology, Department of Medicine and Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA

5 Computer Technologies Department, ITMO University, Saint Petersburg 197101, Russia

6 These authors contributed equally

7 Lead Contact

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https://doi.org/10.1016/j.immuni.2020.11.005

SUMMARY

      Systematic understanding of immune aging on a whole-body scale is currently lacking. We characterized age-associated alterations in immune cells across multiple mouse organs using single-cell RNA and antigen receptor sequencing and flow cytometry-based validation. We defined organ-specific and common immune alterations and identified a subpopulation of age-associated granzyme K (GZMK)-expressing CD8+ T (Taa) cells that are distinct from T effector memory (Tem) cells. Taa cells were highly clonal, had specific epigenetic and transcriptional signatures, developed in response to an aged host environment, and expressed markers of exhaustion and tissue homing. Activated Taa cells were the primary source of GZMK, which enhanced in-flammatory functions of non-immune cells. In humans, proportions of the circulating GZMK+ CD8+ T cell population that shares transcriptional and epigenetic signatures with mouse Taa cells increased during healthy aging. These results identify GZMK+ Taa cells as a potential target to address age-associated dysfunctions of the immune system.

Graphical abstract

Highlights

● A single-cell transcriptomic atlas across aged tissues and their rejuvenation in HP

● HP systemically rejuvenated senile adult stem cells and their niches across tissues

● Youthful transcriptomes were restored in resident HSPCs upon young blood exposure

● Reintroduction of rejuvenating factors in aged HSCs mitigated lymphopoiesis decline

Authors

Shuai Ma, Si Wang, Yanxia Ye, ..., Jing Qu, Weiqi Zhang, Guang-Hui Liu

Correspondence

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In brief

      Ma and colleagues report a multi-tissue single-cell transcriptomic atlas of HP. They reveal that adult stem cells, especially bone marrow HSPCs, are responsive to the changing milieu. Focusing on HSPCs, they uncover HPinduced rejuvenating programs with underlying key mediators, overexpression of which recharges the lymphopoiesis potential of aged HSCs.

Shuai Ma,1,4,7,14,15 Si Wang,3,8,14,15,16 Yanxia Ye,2,4,7,15 Jie Ren,4,5,6,12,15,16 Ruiqing Chen,9,15 Wei Li,3,8,16 Jiaming Li,5,6,12 Liyun Zhao,3,8 Qian Zhao,3,8 Guoqiang Sun,2,6 Ying Jing,2,6 Yuesheng Zuo,5,6 Muzhao Xiong,5,6 Yuanhan Yang,1,6 Qiaoran Wang,5,6 Jinghui Lei,3,8 Shuhui Sun,1,4,7 Xiao Long,11 Moshi Song,1,4,7,16 Shuyang Yu,10,16 Piu Chan,3,16 Jianwei Wang,9,16 Qi Zhou,2,4,6,7,16 Juan Carlos Izpisua Belmonte,13,16 Jing Qu,2,4,6,7, * Weiqi Zhang,4,5,6,7,12,14, * and Guang-Hui Liu1,3,4,6,7,8,17, *

1 State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China

2 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China

3 Advanced Innovation Center for Human Brain Protection and National Clinical Research Center for Geriatric Disorders, Xuanwu Hospital Capital Medical University, Beijing 100053, China

4 Institute for Stem Cell and Regeneration, CAS, Beijing 100101, China

5 CAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences and China National Center for Bioinformation, Beijing 100101, China

6 University of Chinese Academy of Sciences, Beijing 100049, China

7 Beijing Institute for Stem Cell and Regenerative Medicine, Beijing 100101, China

8 Aging Translational Medicine Center, International Center for Aging and Cancer, Beijing Municipal Geriatric Medical Research Center, Xuanwu Hospital, Capital Medical University, Beijing 100053, China

9 School of Pharmaceutical Sciences, Tsinghua University, Beijing 100084, China

10 State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing 100193, China

11 Division of Plastic Surgery, Peking Union Medical College Hospital, Beijing 100032, China

12 Sino-Danish College, University of Chinese Academy of Sciences, Beijing, China

13 Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, CA, USA

14 The Fifth People’s Hospital of Chongqing, Chongqing 400062, China

15 These authors contributed equally

16 Senior author

17 Lead contact

*Correspondence: 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (J.Q.), 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (W.Z.), 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。 (G.-H.L.) https://doi.org/10.1016/j.stem.2022.04.017

SUMMARY

      The young circulatory milieu capable of delaying aging in individual tissues is of interest as rejuvenation strategies, but how it achieves cellular- and systemic-level effects has remained unclear. Here, we constructed a single-cell transcriptomic atlas across aged tissues/organs and their rejuvenation in heterochronic parabiosis (HP), a classical model to study systemic aging. In general, HP rejuvenated adult stem cells and their niches across tissues. In particular, we identified hematopoietic stem and progenitor cells (HSPCs) as one of the most responsive cell types to young blood exposure, from which a continuum of cell state changes across the hematopoietic and immune system emanated, through the restoration of a youthful transcriptional regulatory program and cytokine-mediated cell-cell communications in HSPCs. Moreover, the reintroduction of the identified rejuvenating factors alleviated age-associated lymphopoiesis decline. Overall, we provide comprehensive frameworks to explore aging and rejuvenating trajectories at single-cell resolution and revealed cellular and molecular programs that instruct systemic revitalization by blood-borne factors.