Aleksandra Maciejowska

Ms. Aleksandra Maciejowska


Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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14 October 2025 in Antioxidants
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Journal Article
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MDMagdalena Karolina Dzięgiel
Magdalena Karolina Dzięgiel
AMAleksandra Maciejowska
Aleksandra Maciejowska
MMMarek Misiak
Marek Misiak
Katarzyna LisowskaKatarzyna Lisowska
Katarzyna Lisowska
Smoking cigarettes affects the human body on many levels—not only are the lungs and heart targeted, but also other organs, directly and through derived alterations. We decided to parallel the impacts most often described in the literature in the hope of better future targeting regarding treatment for smoke-induced renal injury. As a result of our research, it is clear that damage is mostly localized directly in vessels and glomeruli. We perceive it as a connected web, where oxidative stress leads to local inflammation, general inflammation in the form of obesity, or inflammation due to nasopharyngeal infection. It later affects other types of tissues: podocytes, epithelium in both glomeruli, renal tubules, and vessels. We mention major molecules proven to participate in kidney damage that tend to be similar in all disease entities depicted in this study: IgA nephropathy, membranous nephropathy, and minimal change disease. Moreover, as nicotine is a major component of both classic cigarettes and electronic cigarettes, we decided to approximate and summarize the information on its impact on primary glomerulopathies.

Verified
Journal Article
Open access
PDF file
MDMagdalena Karolina Dzięgiel
Magdalena Karolina Dzięgiel
MMMarek Misiak
Marek Misiak
AMAleksandra Maciejowska
Aleksandra Maciejowska
Katarzyna LisowskaKatarzyna Lisowska
Katarzyna Lisowska
The influence of gaseous components of tobacco smoke, e-cigarettes, and air pollutants on the development of glomerulonephritis has been the subject of numerous studies in recent years. Glomerulonephritis (GN) often leads to progressive kidney damage and chronic kidney disease (CKD), which is a global health problem. Genetic and autoimmune factors have been shown to contribute to their development. Yet, increasing attention is being given to environmental and lifestyle-related risk factors. This paper summarizes how specific substances found in tobacco smoke, e-cigarette smoke, and air pollutants contribute to the development and progression of GN. Particular emphasis is placed on substances such as formaldehyde, heavy metals, and particulate matter, which have been shown to trigger oxidative stress, immune dysregulation, and endothelial dysfunction. A clear understanding of the contributions of those agents to kidney inflammation is crucial for developing preventive strategies and improving public health awareness. We also highlight gaps in current research and suggest directions for future investigation. Understanding consequences of cigarette smoking should be promoted to encourage people to reduce their exposure to cigarette smoke, which could prevent many diseases.

Verified
Journal Article
Open access
PDF file
MDMagdalena Karolina Dzięgiel
Magdalena Karolina Dzięgiel
AMAleksandra Maciejowska
Aleksandra Maciejowska
DJDawid Juszkiewicz
Dawid Juszkiewicz
WKWiktor Kaleta
Wiktor Kaleta
MZMarta Zawadzka
Marta Zawadzka
MMMaria Mazurkiewicz-Bełdzińska
Maria Mazurkiewicz-Bełdzińska
Worster-Drought syndrome (WDS), also known as congenital suprabulbar paresis, is a rare neurodevelopmental disorder characterized by feeding, swallowing, drooling, and speech disturbances. Currently, it is classified as a subtype of cerebral palsy. However, the limited number of studies and the clinical and radiological overlap with related entities such as congenital bilateral perisylvian syndrome (CBPS) and Foix-Chavany-Marie syndrome (FCMS) have contributed to persistent uncertainty regarding its proper classification. In this review, we summarize the current knowledge on the WDS based on data from published case series. Special emphasis is placed on proposed etiological mechanisms, including recent genetic findings potentially contributing to WDS, as well as on the diagnostic process, ongoing classification dilemmas, and spectrum-based perspective. We point out the need to establish standardized diagnostic criteria and conduct large-scale genetic and neurodevelopmental research. Addressing these gaps may help clarify the underlying pathophysiology, reappraise the classification framework, and ultimately minimize misdiagnosis and time to proper diagnosis to improve outcomes for individuals affected by WDS.