Sulforaphane as a Therapeutic Target for Sarcopenia in Type 2 Diabetes: Mechanistic Insights and Translational Evidence.
4 affiliations
- 1Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa 3886, South Africa.
- 2Department of Biochemistry, North-West University, Mafikeng Campus, Mmabatho 2735, South Africa.
- 3Department of Life and Environmental Sciences, Polytechnic University of Marche, 60131 Ancona, Italy.
- 4School of Medicine, University of KwaZulu-Natal, Durban 4000, South Africa.
Abstract
Sulforaphane, a bioactive isothiocyanate abundant in cruciferous vegetables, has emerged as a potential multi-target therapeutic agent capable of mitigating these pathological processes. Here, using evidence from preclinical and clinical literature, we review the mechanistic and translational evidence linking sulforaphane with the preservation of skeletal muscle tissue in the context of sarcopenia associated with T2D. The reviewed evidence suggests sulforaphane modulates oxidative stress, inflammation, and mitochondrial dysfunction through activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and related signaling pathways. Preclinical rodent studies corroborate these findings, reporting improved muscle mass, contractility, metabolic homeostasis, and attenuation of inflammation via Nrf2/heme oxygenase (HO)-1, AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) pathways. Limited clinical evidence from two small studies in healthy adults suggest that short-term sulforaphane supplementation (30 mg/day) may reduce exercise-induced muscle damage and enhance antioxidant responses. The evidence collectively highlights sulforaphane as a promising candidate for preserving skeletal muscle integrity in T2D. However, more randomized controlled trials are required to define optimal dosing, long-term safety, and direct efficacy in patients with sarcopenia and diabetes. This review strengthens the translational value of sulforaphane while integrating mechanistic insights and therapeutic potential against T2D-associated sarcopenia.
Related
- Circular RNAs in Skeletal Muscle Aging and Sarcopenia: Mechanistic Evidence, Biomarker Potential, and Therapeutic Readiness
- CRISPR Technologies in Type 2 Diabetes: From Mechanistic Insights to Therapeutic Discovery
- Single-cell Transcriptomics in Autoimmune Diseases: Mechanistic Insights, Cross-disease Convergence, and Translational Challenges in Rheumatoid Arthritis, Systemic Lupus Erythematosus, Type 1 Diabetes, and Multiple Sclerosis.
- Dynamic three-dimensional chromatin remodeling in lung disease: mechanistic principles, pathogenic regulatory networks, and translational challenges
- Natural Products in Anticancer Activity: 2nd Edition—From Chemical Diversity to Mechanistic and Translational Insights
BibTeX
@article{ngcobo2026sulforaphane,
title = {{Sulforaphane as a Therapeutic Target for Sarcopenia in Type 2 Diabetes: Mechanistic Insights and Translational Evidence.}},
author = {Ayanda Ngcobo and Samukelisiwe C Shabalala and Nokulunga Hlengwa and Ndivhuwo Muvhulawa and Patrick Orlando and Sonia Silvestri and Luca Tiano and Phiwayinkosi V Dludla},
journal = {Antioxidants (Basel, Switzerland)},
year = {2026},
month = oct,
doi = {10.3390/antiox15101272},
url = {https://europepmc.org/article/MED/42939845},
note = {CC BY},
}
RIS
TY - JOUR
TI - Sulforaphane as a Therapeutic Target for Sarcopenia in Type 2 Diabetes: Mechanistic Insights and Translational Evidence.
AU - Ayanda Ngcobo
AU - Samukelisiwe C Shabalala
AU - Nokulunga Hlengwa
AU - Ndivhuwo Muvhulawa
AU - Patrick Orlando
AU - Sonia Silvestri
AU - Luca Tiano
AU - Phiwayinkosi V Dludla
PY - 2026
DA - 2026/10/02
JO - Antioxidants (Basel, Switzerland)
DO - 10.3390/antiox15101272
UR - https://europepmc.org/article/MED/42939845
AB - Sulforaphane, a bioactive isothiocyanate abundant in cruciferous vegetables, has emerged as a potential multi-target therapeutic agent capable of mitigating these pathological processes. Here, using evidence from preclinical and clinical literature, we review the mechanistic and translational evidence linking sulforaphane with the preservation of skeletal muscle tissue in the context of sarcopenia associated with T2D. The reviewed evidence suggests sulforaphane modulates oxidative stress, inflammation, and mitochondrial dysfunction through activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and related signaling pathways. Preclinical rodent studies corroborate these findings, reporting improved muscle mass, contractility, metabolic homeostasis, and attenuation of inflammation via Nrf2/heme oxygenase (HO)-1, AMP-activated protein kinase (AMPK), and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) pathways. Limited clinical evidence from two small studies in healthy adults suggest that short-term sulforaphane supplementation (30 mg/day) may reduce exercise-induced muscle damage and enhance antioxidant responses. The evidence collectively highlights sulforaphane as a promising candidate for preserving skeletal muscle integrity in T2D. However, more randomized controlled trials are required to define optimal dosing, long-term safety, and direct efficacy in patients with sarcopenia and diabetes. This review strengthens the translational value of sulforaphane while integrating mechanistic insights and therapeutic potential against T2D-associated sarcopenia.
SN - 2076-3921
ER -