ReviewFrontiers in endocrinology2023
From mitochondria to sarcopenia: role of 17β-estradiol and testosterone.
Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Association Between Non-traditional Lipid Indices and Sarcopenia: Evidence from a Prospective Chinese Cohort Study.Current medical science · 2026Article
- Muscle mitochondria, function, mass, and quality of life in prostate cancer during androgen deprivation therapy.Nature communications · 2026Article
- Emerging roles of epigenetics in the pathogenesis of sarcopenia.Epigenomics · 2026Review
- Sex-dependent differences in bioenergetics of young mouse brain microvasculature: implications for oxygen-glucose deprivation and reoxygenation injury.American journal of physiology. Heart and circulatory physiology · 2026Article
- Research progress on the molecular mechanism and clinical evidence of glucagon-like peptide-1 receptor agonists in improving sarcopenia.Diabetology & metabolic syndrome · 2026Review
- Sarcopenia in the Aging Process: Pathophysiological Mechanisms, Clinical Implications, and Emerging Therapeutic Approaches.International journal of molecular sciences · 2025Review
- Mitochondrial DNA Deletions and Plasma GDF-15 Protein Levels Are Linked to Hormonal Dysregulation and Multi-Organ Involvement in Female Reproductive Endocrine Disorders.Life (Basel, Switzerland) · 2025Article
- Microenvironment-driven satellite cell regeneration and repair in aging-related sarcopenia: mechanisms and therapeutic frontiers.Stem cell research & therapy · 2025Review
- Potential therapeutic role of sex steroids in treating sarcopenia: a network pharmacology and molecular dynamics study.BMC pharmacology & toxicology · 2025Article
- Review
- Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis.Metabolites · 2025Review
- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
- Review
- Correlation and predictive value of novel anthropometric indicators with adult sarcopenia and sarcopenia obesity.Scientific reports · 2024Article
- Inhibition of CILP2 Improves Glucose Metabolism and Mitochondrial Dysfunction in Sarcopenia via the Wnt Signalling Pathway.Journal of cachexia, sarcopenia and muscle · 2024Article
- The association between testosterone, estradiol, estrogen sulfotransferase and idiopathic pulmonary fibrosis: a bidirectional mendelian randomization study.BMC pulmonary medicine · 2024Article
- Cancerous Conditions Accelerate the Aging of Skeletal Muscle via Mitochondrial DNA Damage.International journal of molecular sciences · 2024Article
- Skeletal Muscle Energetics Explain the Sex Disparity in Mobility Impairment in the Study of Muscle, Mobility and Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- The Current Landscape of Pharmacotherapies for Sarcopenia.Drugs & aging · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sarcopenia, characterized by a loss of muscle mass and strength with aging, is prevalent in older adults. Although the exact mechanisms underlying sarcopenia are not fully understood, evidence suggests that the loss of mitochondrial integrity in skeletal myocytes has emerged as a pivotal contributor to the complex etiology of sarcopenia. Mitochondria are the primary source of ATP production and are also involved in generating reactive oxygen species (ROS), regulating ion signals, and initiating apoptosis signals in muscle cells. The accumulation of damaged mitochondria due to age-related impairments in any of the mitochondrial quality control (MQC) processes, such as proteostasis, biogenesis, dynamics, and mitophagy, can contribute to the decline in muscle mass and strength associated with aging. Interestingly, a decrease in sex hormones (e.g., 17β-estradiol and testosterone), which occurs with aging, has also been linked to sarcopenia. Indeed, 17β-estradiol and testosterone targeted mitochondria and exhibited activities in regulating mitochondrial functions. Here, we overview the current literature on the key mechanisms by which mitochondrial dysfunction contribute to the development and progression of sarcopenia and the potential modulatory effects of 17β-estradiol and testosterone on mitochondrial function in this context. The advance in its understanding will facilitate the development of potential therapeutic agents to mitigate and manage sarcopenia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.