ArticleKidney international2019
Mitochondrial biogenesis induced by the β2-adrenergic receptor agonist formoterol accelerates podocyte recovery from glomerular injury.
Article in Kidney international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 63 citations in OpenAlex.
- Beta 2-adrenergic pathway combats Alzheimer's disease: Restoring cognition and synaptic integrity.Neural regeneration research · 2026Article
- Norepinephrine attenuates acute lung injury by protecting mitochondria via the βRedox biology · 2026Article
- Norepinephrine regulates hippocampal mitochondrial biogenesis via β2-adrenergic receptor signaling and PGC-1α.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Kidney-Targeted Nanoparticle Delivery of Formoterol Mitigates Diabetic Kidney Disease without Adverse Cardiac Effects.ACS pharmacology & translational science · 2026Article
- Extracellular vesicle-derived TMEM106A participated in podocyte injury via EGR1 in preeclampsia.Cellular and molecular life sciences : CMLS · 2026Article
- The βBritish journal of pharmacology · 2026Article
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- Beta 2 adrenergic receptor agonists as a treatment for metabolic dysfunction-associated steatohepatitis (MASH).npj metabolic health and disease · 2026Article
- 5-Hydroxytryptamine 1F receptor loss reduces renal vasculature and prevents lasmiditan-induced recovery following moderate-severe acute kidney injury in mice.American journal of physiology. Renal physiology · 2025Article
- Targeting mitochondrial dysfunction: an innovative strategy for treating renal fibrosis.Molecular and cellular biochemistry · 2025Review
- Enhancing Mitochondrial Function Through Pharmacological Modification: A Novel Approach to Mitochondrial Transplantation in a Sepsis Model.Biomedicines · 2025Article
- Repurposing mitochondria-targeted therapeutics for kidney diseases.Kidney international · 2025Review
- Lasmiditan induces mitochondrial biogenesis in primary mouse renal peritubular endothelial cells and augments wound healing and tubular network formation.American journal of physiology. Cell physiology · 2025Article
- Podocytes in health and glomerular disease.Frontiers in cell and developmental biology · 2025Review
- Unraveling the role of mitochondrial dysfunction in diabetic kidney disease: insights and interventions.Frontiers in pharmacology · 2025Review
- Formoterol promotes mitochondrial biogenesis, improves liver regeneration, and suppresses liver injury and inflammation after liver resection in mice with endotoxemia.International journal of physiology, pathophysiology and pharmacology · 2025Article
- βBiochemistry research international · 2025Review
- Role of the βPharmacological reports : PR · 2024Article
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- βAmerican journal of physiology. Renal physiology · 2024Article
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
Podocytes have limited ability to recover from injury. Here, we demonstrate that increased mitochondrial biogenesis, to meet the metabolic and energy demand of a cell, accelerates podocyte recovery from injury. Analysis of events induced during podocyte injury and recovery showed marked upregulation of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), a transcriptional co-activator of mitochondrial biogenesis, and key components of the mitochondrial electron transport chain. To evaluate our hypothesis that increasing mitochondrial biogenesis enhanced podocyte recovery from injury, we treated injured podocytes with formoterol, a potent, specific, and long-acting β2-adrenergic receptor agonist that induces mitochondrial biogenesis in vitro and in vivo. Formoterol increased mitochondrial biogenesis and restored mitochondrial morphology and the injury-induced changes to the organization of the actin cytoskeleton in podocytes. Importantly, β2-adrenergic receptors were found to be present on podocyte membranes. Their knockdown attenuated formoterol-induced mitochondrial biogenesis. To determine the potential clinical relevance of these findings, mouse models of acute nephrotoxic serum nephritis and chronic (Adriamycin [doxorubicin]) glomerulopathy were used. Mice were treated with formoterol post-injury when glomerular dysfunction was established. Strikingly, formoterol accelerated the recovery of glomerular function by reducing proteinuria and ameliorating kidney pathology. Furthermore, formoterol treatment reduced cellular apoptosis and increased the expression of the mitochondrial biogenesis marker PGC-1α and multiple electron transport chain proteins. Thus, our results support β2-adrenergic receptors as novel therapeutic targets and formoterol as a therapeutic compound for treating podocytopathies.
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