Mostafa Haghpanah

Dr. Mostafa Haghpanah

orcid

Research Focus & Metrics

Academic Career Length

3Years (2024-Present)

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

Representative Publications

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23 October 2024 in Plants
Verified
Journal Article
Open access
PDF file
Mostafa HaghpanahMostafa Haghpanah
Mostafa Haghpanah
SHSeyyed Hamidreza Hashemipetroudi
Seyyed Hamidreza Hashemipetroudi
Ahmad ArzaniAhmad Arzani
Ahmad Arzani
Fabrizio AranitiFabrizio Araniti
Fabrizio Araniti
Drought, a significant environmental challenge, presents a substantial risk to worldwide agriculture and the security of food supplies. In response, plants can perceive stimuli from their environment and activate defense pathways via various modulating networks to cope with stress. Drought tolerance, a multifaceted attribute, can be dissected into distinct contributing mechanisms and factors. Osmotic stress, dehydration stress, dysfunction of plasma and endosome membranes, loss of cellular turgidity, inhibition of metabolite synthesis, cellular energy depletion, impaired chloroplast function, and oxidative stress are among the most critical consequences of drought on plant cells. Understanding the intricate interplay of these physiological and molecular responses provides insights into the adaptive strategies plants employ to navigate through drought stress. Plant cells express various mechanisms to withstand and reverse the cellular effects of drought stress. These mechanisms include osmotic adjustment to preserve cellular turgor, synthesis of protective proteins like dehydrins, and triggering antioxidant systems to counterbalance oxidative stress. A better understanding of drought tolerance is crucial for devising specific methods to improve crop resilience and promote sustainable agricultural practices in environments with limited water resources. This review explores the physiological and molecular responses employed by plants to address the challenges of drought stress.

25 April 2025 in Plants
Verified
Journal Article
Open access
PDF file
Mostafa HaghpanahMostafa Haghpanah
Mostafa Haghpanah
ANAmin Namdari
Amin Namdari
MKmostafa koozehgar kaleji
mostafa koozehgar kaleji
Azam Nikbakht-DehkordiAzam Nikbakht-Dehkordi
Azam Nikbakht-Dehkordi
Ahmad ArzaniAhmad Arzani
Ahmad Arzani
Fabrizio AranitiFabrizio Araniti
Fabrizio Araniti
Reactive oxygen species (ROS) are toxic by-products of aerobic cellular metabolism. However, ROS conduct multiple functions, and specific ROS sources can have beneficial or detrimental effects on plant health. This review explores the complex dynamics of ROS in plant defense mechanisms, focusing on their involvement in basal resistance, hypersensitive response (HR), and systemic acquired resistance (SAR). ROS, including superoxide anion (O2−), singlet oxygen (1O2), hydroxyl radicals (OH), and hydrogen peroxide (H2O2), are generated through various enzymatic pathways. They may serve to inhibit pathogen growth while also activating defense-related gene expression as signaling molecules. Oxidative damage in cells is mainly attributed to excess ROS production. ROS produce metabolic intermediates that are involved in various signaling pathways. The oxidative burst triggered by pathogen recognition initiates hyper-resistance (HR), a localized programmed cell death restricting pathogen spread. Additionally, ROS facilitate the establishment of SAR by inducing systemic signaling networks that enhance resistance across the plant. The interplay between ROS and phytohormones such as jasmonic acid (JA), salicylic acid (SA), and ethylene (ET) further complicates this regulatory framework, underscoring the importance of ROS in orchestrating both local and systemic defense responses. Grasping these mechanisms is essential for creating strategies that enhance plant resilience to biotic stresses.

11 March 2025 in Physiological and Molecular Plant Pathology
Verified
Journal Article
Closed access
Mostafa HaghpanahMostafa Haghpanah
Mostafa Haghpanah
NJNadali Babaeian Jelodar
Nadali Babaeian Jelodar
HZHamid Najafi Zarrini
Hamid Najafi Zarrini
APAli Pakdin-Parizi
Ali Pakdin-Parizi
Ali DehestaniAli Dehestani
Ali Dehestani