ArticleAging advances2025
Narrative review of mitochondrial dysfunction in aging-related salt-sensitive hypertension: outcomes, mechanisms, and therapeutic implications.
Article in Aging advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Melatonin Targets Mitochondrial Redox Homeostasis: Optimizing the Intracellular Microenvironment.International journal of molecular sciences · 2026Review
- Redox-Regulated Mitophagy and Lysosomal Dysfunction as a Convergent Mechanism in Female Infertility: Molecular Insights and Therapeutic Perspectives.Current issues in molecular biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
Salt sensitivity of blood pressure is prevalent in the aging population, characterized by an exaggerated hypertensive response to dietary sodium intake. Emerging evidence implicates mitochondrial dysfunction as a central contributor to salt sensitivity of blood pressure with mechanistic involvement of oxidative stress, endoplasmic reticulum stress, disrupted mitochondrial-endoplasmic reticulum contacts, and impaired autophagy. This review explores the interplay between aging, mitochondrial dysfunction, and salt sensitivity of blood pressure. Morphological mitochondrial changes including mitochondrial fragmentation due to fission-fusion imbalances, cristae remodeling leading to bioenergetic deficits, and mitochondrial-endoplasmic reticulum contact disruptions affecting calcium homeostasis across aging are contextualized in salt sensitivity of blood pressure. Alongside these changes, age-associated impairments in mitophagy result in the accumulation of defective mitochondria, exacerbating oxidative stress and inflammation. Understanding these pathways offers potential therapeutic avenues to attenuate salt sensitivity of blood pressure in older adults.
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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 Socratic graph.