ReviewThe Yale journal of biology and medicine2026
Mitochondrial Dysfunction in Renal Proximal Tubule Injury: Mechanisms, Pathophysiology, and Therapeutic Opportunities.
Review in The Yale journal of biology and medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria play a key role in both health and disease. Mitochondrial dysfunction, characterized by oxidative stress, impaired bioenergetics, altered dynamics, defective mitophagy, and mitochondrial DNA-mediated signaling, is critically involved in both acute kidney injury and chronic kidney disease. These defects not only trigger tubular cell death, but also drive inflammation, fibrosis, and maladaptive remodeling through interactions with endoplasmic reticulum stress, metabolic pathways, and epithelial-to-mesenchymal transition. This review summarizes the structure and function of mitochondria in the renal proximal tubules and outlines the most prominent mechanisms contributing to mitochondrial dysfunction in tubular injury. Because mitochondria play a central role in renal pathophysiology, therapies targeting mitochondria have emerged as promising strategies for preventing and treating kidney disease. Here, we review emerging therapeutic options aimed at improving mitochondrial function, including mitochondria-targeted antioxidants, metabolic modulators and activators of the AMP-activated protein kinase and sirtuins, modulators of mitochondrial fission and fusion, enhancers of mitophagy, gene-based approaches, and stem cell- or exosome-based therapies. There is growing evidence that multitargeting mitochondria by combining different pathways may offer more effective protection against tubular injury and the progression of tubular disease. Finally, future perspectives and translational challenges are discussed, including the definition of reliable mitochondrial biomarkers, development of organ-specific delivery systems, application of precision medicine approaches, and long-term safety considerations. Collectively, mitochondrial defects in renal tubule injury represent a promising target for innovative, organelle-centered strategies to safeguard kidney function.
Indexed as
Identifiers
What OpenQuestion holds
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.