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Showing 1–22 of 22 results
Advanced filters: Author: Sundeep Khosla Clear advanced filters

  • In this Review, Joshua Farr and Sundeep Khosla discuss changes in bone architecture during growth, placing an emphasis on skeletal changes at the distal radius, a clinically relevant site of forearm fractures. The implications of these changes for fracture risk in adolescence and later in life, and the architectural changes in bone with ageing that might contribute to increased fracture risk are also discussed.

    • Joshua N. Farr
    • Sundeep Khosla
    Reviews
    Nature Reviews Endocrinology
    Volume: 11, P: 513-521

  • Attempts to translate senolytics from preclinical models to humans are gaining momentum. Early clinical trials have provided positive biological signals, but we lack clear evidence for the efficacy of senolytics in humans. Based on what we have learned in these initial trials, it may be time to aim for a more personalized approach in designing future senolytic trials, and potentially also in the eventual clinical use of these compounds.

    • Sundeep Khosla
    • David G. Monroe
    • Joshua N. Farr
    Comments & Opinion
    Nature Aging
    Volume: 5, P: 1926-1929

  • Romosozumab, a recently developed sclerostin inhibitor, stimulates bone formation and inhibits bone resorption, thereby markedly increasing bone mass and reducing fracture risk. But will a red flag regarding possible adverse cardiovascular events derail this promising new drug for osteoporosis?

    • Sundeep Khosla
    News & Views
    Nature Reviews Endocrinology
    Volume: 13, P: 697-698

    • Sundeep Khosla
    Comments & Opinion
    Nature Medicine
    Volume: 17, P: 430-431

  • Anti-resorptive bone therapies also inhibit bone formation, as osteoclasts secrete factors that stimulate bone formation by osteoblasts. Here, the authors identify osteoclast-secreted factors that couple bone resorption to bone formation in healthy subjects, and show that osteoclast-derived DPP4 may be a factor coupling bone resorption to energy metabolism.

    • Megan M. Weivoda
    • Chee Kian Chew
    • Sundeep Khosla
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-13

  • There is tremendous interest in the development of drugs that target senescent cells (‘senolytic’ drugs) to treat a range of age-related morbidities. However, studies in mice that demonstrate impaired tissue repair following clearance of senescent cells raise questions about the potential risks of senolytic therapies. Closer examination of the available studies reveals the hopeful possibility of a ‘therapeutic window’ in which these risks can be minimized.

    • Sundeep Khosla
    Comments & Opinion
    Nature Aging
    Volume: 3, P: 139-141

  • During senescence, minority mitochondrial outer membrane permeabilization leads to the release of mtDNA into the cytosol through BAX and BAK macropores, in turn activating the cGAS–STING pathway, a major regulator of the senescence-associated secretory phenotype.

    • Stella Victorelli
    • Hanna Salmonowicz
    • João F. Passos
    ResearchOpen Access
    Nature
    Volume: 622, P: 627-636

  • Senescent cells accumulate with age and contribute to the functional decline of many tissues; however, their role in skeletal muscle is not well understood. Here the authors comprehensively assess cellular senescence in skeletal muscle of young and old mice and detail senescence features in subpopulations of p16+ fibroadipogenic progenitors and p21+ myofibers.

    • Xu Zhang
    • Leena Habiballa
    • Nathan K. LeBrasseur
    Research
    Nature Aging
    Volume: 2, P: 601-615

  • Senescent cells have complex and important roles in cancer and ageing, but they are quite rare and difficult to characterize in tissues in vivo. In this Expert Recommendation, the SenNet Biomarkers Working Group discusses recent advances in detecting and characterizing cellular senescence and provides recommendations for senescence markers in 14 human and mouse tissues.

    • Vidyani Suryadevara
    • Adam D. Hudgins
    • Nicola Neretti
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 25, P: 1001-1023

  • Transfer of senescent cells into naive, young mice can induce physical dysfunction, and a senolytic can reverse this dysfunction and potently increase lifespan in aged mice.

    • Ming Xu
    • Tamar Pirtskhalava
    • James L. Kirkland
    Research
    Nature Medicine
    Volume: 24, P: 1246-1256

  • This Review outlines the pathogenesis of skeletal fragility in patients with type 2 diabetes mellitus, and discusses potential therapeutic approaches to the management of increased fracture risk in these patients. The evidence that skeletal fragility should now be included in the list of well-recognized diabetic complications is also summarized.

    • Sundeep Khosla
    • Parinya Samakkarnthai
    • Joshua N. Farr
    Reviews
    Nature Reviews Endocrinology
    Volume: 17, P: 685-697

  • Current drugs for osteoporosis primarily prevent bone loss, and there is a substantial need for treatments that could reduce fracture risk further. Rosen and colleagues describe recent insights into skeletal physiology that are providing the basis for novel therapeutics to promote bone formation, and discuss the regulatory and commercial challenges for these agents.

    • Masanobu Kawai
    • Ulrike I. Mödder
    • Clifford J. Rosen
    Reviews
    Nature Reviews Drug Discovery
    Volume: 10, P: 141-156

  • The COVID-19 pandemic has broad implications for the care of patients with bone fragility. A dramatic surge in fractures and related mortality is expected in the next few months. We pledge to intensify the current efforts to improve the management of bone health, and to prioritize fragility fracture care and prevention.

    • Nicola Napoli
    • Ann L. Elderkin
    • Sundeep Khosla
    Comments & Opinion
    Nature Reviews Endocrinology
    Volume: 16, P: 467-468

  • This Review discusses mechanisms of cellular senescence and approaches to target this pathway therapeutically using ‘senolytic’ drugs or inhibitors of the senescence-associated secretory phenotype. In addition, evidence is presented that cellular senescence has a causative role in multiple chronic diseases associated with ageing and/or endocrine diseases.

    • Sundeep Khosla
    • Joshua N. Farr
    • James L. Kirkland
    Reviews
    Nature Reviews Endocrinology
    Volume: 16, P: 263-275