Sabin Khadgi Data-verified
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Biography and Research Information
OverviewAI-generated summary
Sabin Khadgi's research focuses on the molecular and cellular adaptations of skeletal muscle, particularly in response to exercise and during conditions such as cancer cachexia. His work investigates the temporal molecular changes occurring in muscle tissue over a 24-hour period following stimuli like resistance exercise, identifying key regulatory factors such as MYC as sufficient for muscle growth. Khadgi also studies the impact of aging on exercise adaptation and explores therapeutic strategies, including mitochondrial antioxidants like SkQ1 and promoting mitochondrial fusion, to counteract muscle wasting associated with cancer and aging. His publications have examined these processes in both human and animal models, including mice, and have identified immune cell involvement in muscle regeneration during mechanical loading in geriatric populations. Khadgi has a h-index of 6 with 164 total citations across 14 publications.
Metrics
- h-index: 6
- Publications: 14
- Citations: 169
Selected Publications
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Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females (2025)
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Satellite cells choreograph an immune cell-fibrogenic cell circuit during mechanical loading in geriatric skeletal muscle (2025)
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Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice (2025)
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Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice (2025)
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The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth (2024)
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Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice (2024)
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Precision and efficacy of RNA-guided DNA integration in high-expressing muscle loci (2024)
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The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth (2024)
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A Rejuvenation Signature in Skeletal Muscle That Is Mediated By Late-Life Exercise (2023)
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A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle (2022)
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Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks (2022)
Collaboration Network
Top Collaborators
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Showing 5 of 12 shared publications
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Showing 5 of 10 shared publications
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
Showing 5 of 10 shared publications
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- A Rejuvenation Signature in Skeletal Muscle That Is Mediated By Late-Life Exercise
Showing 5 of 7 shared publications
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Satellite cells choreograph an immune cell-fibrogenic cell circuit during mechanical loading in geriatric skeletal muscle
Showing 5 of 6 shared publications
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- A Rejuvenation Signature in Skeletal Muscle That Is Mediated By Late-Life Exercise
- Mitochondria-Targeted Antioxidant SkQ1 Improves Muscle Contractility in Female C26 Tumor-Bearing Mice
- A molecular signature defining exercise adaptation with ageing and <i>in vivo</i> partial reprogramming in skeletal muscle
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Satellite cells choreograph an immune cell-fibrogenic cell circuit during mechanical loading in geriatric skeletal muscle
- A Rejuvenation Signature in Skeletal Muscle That Is Mediated By Late-Life Exercise
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Mitochondria-Targeted Antioxidant SkQ1 Improves Muscle Contractility in Female C26 Tumor-Bearing Mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Mitochondria-Targeted Antioxidant SkQ1 Improves Muscle Contractility in Female C26 Tumor-Bearing Mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- Mitochondrial antioxidant SkQ1 attenuates C26 cancer-induced muscle wasting in males and improves muscle contractility in female tumor-bearing mice
- Promoting mitochondrial fusion is protective against cancer-induced muscle detriments in males and females
- Myocellular adaptations to short‐term weighted wheel‐running exercise are largely conserved during C26‐tumour induction in male and female mice
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
- Multi-transcriptome analysis following an acute skeletal muscle growth stimulus yields tools for discerning global and MYC regulatory networks
- The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth
- The 24-Hour Time Course of Integrated Molecular Responses to Resistance Exercise in Human Skeletal Muscle Implicates <i>MYC</i> as a Hypertrophic Regulator That is Sufficient for Growth
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